Topic Guide

Acute Pulmonary Infections

Bacterial Pneumonias
Klebsiella (Friedlnder's) Pneumonia
Streptococcus pyogenes Pneumonia
Pseudomonas Pneumonia
Viral, Mycoplasmal, and Rickettsial Pneumonias
Chlamydia trachomatis Pneumonia
Other Infections
Pulmonary Cystic Fibrosis (Mucoviscidosis)

Topic Guide
Pulmonary Tuberculosis
General Considerations
Primary Pulmonary Tuberculosis
Postprimary (Reinfection, Reactivation) Tuberculosis
Bronchiectasis
Unusual Radiographic Manifestations of Pulmonary Tuberculosis
Tuberculosis in the Immunosuppressed Patient
Tuberculoma
Healing of Pulmonary Tuberculosis
Complications of Reinfection Pulmonary Tuberculosis
Hematogenous Tuberculosis
Miliary Pulmonary Tuberculosis
Subacute and Chronic Hematogenous Pulmonary Dissemination
Atypical Mycobacteria
Surgical Measures in Pulmonary Tuberculosis
Complicating Aspergillomas

Topic Guide
Actinomycosis
Nocardiosis
Mycotic Diseases of the Lung
Coccidioidomycosis
Histoplasmosis
Cryptococcosis
North American Blastomycosis
South American Blastomycosis (Paracoccidioidomycosis)
Pulmonary Aspergillosis
Moniliasis (Candidiasis)
Geotrichosis
Other Mycoses

Topic Guide
Diseases of Spirochetal Origin
Syphilis
Leptospirosis
Protozoan Diseases
Amebiasis
Toxoplasmosis
Platyhelminth (Flatworm) Infestation
Echinococcosis (Hydatid Disease)
Cysticercosis
Paragonimiasis
Schistosomiasis
Nemathelminth (Roundworm) Infestation
Tropical Eosinophilia

ACUTE PULMONARY INFECTIONS

Type

Organism

Characeristics

Roentgen Pattern

Lobar
(alveolar, airspace)
pneumonia

Streptococcu
s
pneumoniae
pneumonia.

Periphery of the lung via the

airways.

peripheral homogeneous (consolidation)

opacity spreads toward the hilum and
tends to cross segmental lines.

Alveolar transudation (edema) is

followed by migration of leukocytes
into the alveolar fluid.

Alveolar pneumonia is not necessarily

confined to a lobe, nor does it involve an
entire lobe in many instances.

Lobar is a misnomer in most

cases.
Bronchopneu
monia
(lobular
pneumonia).

staphylococc
al infection
of the lung.

Acute
interstitial
pneumonia

virus or a
mycoplasma

Mixed
pneumonia

Originates in the airways and

spreads to peribronchial alveoli.
Confined by interlobular septa.

Interstitial involvement is masked

by alveolar exudate
This is a combination of lobar,
bronchopneumonia, and interstitial
pneumonia

patchy disease causing poorly defined

opacities
a variety of roentgen patterns may
result,
including
a
confluent
consolidation resembling lobar (alveolar)
pneumonia.
alveolar consolidation, if present, is not
usually as confluent or as dense as in
lobar or lobular pneumonia

Bacterial Pneumonias
Pneumococcal Pneumonia

S. pneumoniae

caused by types 1, 3, 4, 5, 7, 8, 9, or 12.

Type 8 is the most common.
Type 14 causes pneumonia in children but rarely in adults.
The mortality rate for pneumonia caused by type 3 is higher than for
the others.

lobar pneumonia
generally more severe in those with alcoholism, neoplastic
disease, chronic pulmonary disease, or altered immunity.
lower lobes and posterior segments of upper lobes are most
commonly involved.
The onset is sudden
gross pathologic changes are evident early in the disease
roentgen findings can be observed within 6 to 12 hours
after onset of symptoms.

Pneumococcal Pneumonia

Involvement
usually
begins
peripherally
and
spreads
centripetally
with
homogeneous
involvement that may
cross
segmental
boundaries.
Consolidation:
homogeneous density.
An entire lobe may be
affected;
more
commonly only one or
a few segments are
involved.
Density
usually
extends to the pleural
surface.
A
peripheral,
nonsegmental,

Lobar pneumonia in the right middle lobe. Note the

homogeneous opacity clearly defined by the secondary
fissure in the frontal projection ( A) and by the major
fissure as well as the secondary fissure in the lateral view
( B).

Pneumococcal Pneumonia

all of the elements in the

diseased lobe except the
larger bronchi may be
affected,
resulting
in
almost
complete
airlessness.
Larger bronchi: seen as
air-containing,
radiolucent tubes within
the
otherwise
homogeneous
density,
the air bronchogram.
Pleural
involvement:
elevation
of
the
hemidiaphragm on the
affected side.
Pleural fluid: sufficient to
obscure the depth of the
costophrenic sulcus.
Opacity caused by this
disease
can
be
differentiated from that

Right-upper-lobe
pneumococcal
pneumonia.
A:
Roentgenogram obtained the day after onset of symptoms
shows the disease clearly defined by the minor fissure.
Consolidation is not complete. B: Three days later, there is
complete consolidation of the right upper lobe. The upperlobe volume is slightly reduced, but there is no significant
collapse.

Pneumococcal Pneumonia
The spherical pattern
(round
pneumonia)
often
reported
in
children is a form in
which
the
wellcircumscribed
spherical consolidation
may
simulate
a
pulmonary
or
paramediastinal mass.

Frontal view of the chest shows a rounded

soft-tissue density in the posterolateral
aspects of both lower lobes with mild
bilateral hilar prominence.

Pneumococcal Pneumonia
In patients with
emphysema,
radiolucent blebs
surrounded
by
consolidation may
simulate cavities.
In some patients,
the distribution of
the
disease
is
somewhat patchy
or
lobular,
simulating
the
distribution
in
bronchopneumoni
a.

Bronchopneumonia

usually occurs as a complication of various debilitating diseases, often at the extremes of life.
It is most commonly found in the very young or very old who are afflicted with another disease.
The infection is often mixed, so that several pathogenic bacteria can be isolated from the sputum.
The disease originates in numerous adjacent areas of the lung, resulting in scattered foci of inflammation
that vary in size and shape but produce enough density to be visible on the film.
The inflammatory disease does not cross septal boundaries. Therefore, the pattern of disease is
discontinuous or patchy.
The pneumonic consolidation causes densities of varying sizes that are usually rather small and poorly
defined and may be described as mottled.
The location is usually basal, but disease may occur anywhere in the lung.
It often occurs as a complication of another pulmonary disease, which may obscure the pneumonia or vice
versa.
It is particularly difficult to define and diagnose when it occurs as a complication in cardiac failure with
pulmonary congestion and edema, which also cause basal opacity.
It is also difficult to differentiate from other acute or subacute pulmonary diseases such as adult
respiratory distress syndrome (ARDS).
Occasionally, the process is extremely widespread and simulates miliary pulmonary disease, with small,
poorly defined nodules scattered uniformly throughout both lungs.
In contrast to alveolar pneumonia, bronchopneumonia originates in the bronchial airways and involves the
surrounding parenchyma.
As indicated, it may become confluent and then resemble alveolar pneumonia.
It should be remembered that neoplasms can be masked by patchy focal pneumonia, and if clinical
symptoms persist unduly, progress roentgenograms as well as cytologic studies should be recommended.

Bronchopneumonia
Note
that
the
widespread,
mottled opacity is
more severe on
the left than on
the
right.
The
disease is very
extensive.

Aspiration Pneumonia
Aspiration pneumonia is usually a mixed bacterial infection caused by aspiration of foreign
material into the bronchial tree. The causes are numerous and range from aspiration of vomitus
by a postsurgical or semicomatose patient to aspiration as a result of paresis or paralysis of the
pharyngeal muscles.
Tracheoesophageal fistula, gastroesophageal reflux, and various other esophageal lesions can
also cause aspiration pneumonitis. Gram-negative organisms included in the aspirate may
produce pneumonia followed by necrosis and abscess formation.130 This complication is
discussed in the section on lung abscess.
The radiographic findings vary with the extent of disease and its location. The right lower and
middle lobes are most frequently affected, but involvement of the left lower lobe is not unusual.
Irregular, poorly defined areas of increased density are seen and may be extensive ( Fig. 24-4).
Early in the disease these densities are focal, but later they may become conglomerate. In
some instances the disease is acute and clears rapidly as the patient recovers from the
condition that produced the aspiration. In other instances the pneumonia results from a chronic
disease, and repeated aspiration leads to chronic basal pneumonitis, which causes patchy or
linear basal opacity (Fig. 24-5 and Fig. 24-6). Aspiration of acid-containing gastric contents
(Mendelson's syndrome), can produce a chemical pneumonitis causing pulmonary edema, often
in a dependent portion of one or both lungs. The appearance is similar to basal pulmonary
edema of other causes. The roentgen findings are therefore varied, and it may not be possible
to differentiate this basal inflammatory disease from other nonspecific basal pneumonia or from
the chronic pneumonia associated with bronchiectasis. However, correlation of the history with
clinical and roentgen findings usually leads to the proper diagnosis.

Aspiration pneumonia
Note
the
scattered patchy
opacities in the
lower half of the
left lung and a
similar but less
extensive change
at the right base.
This was an acute
process
that
cleared quickly on
treatment.

Chronic aspiration
pneumonia
The pneumonia in the
parahilar areas and at
the right base is
somewhat
more
clearly defined and
stringy than the acute
process. This patient
had
partial
esophageal
obstruction and had
aspirated
intermittently
for
several months.

Chronic Recurrent Aspiration

A
and
B:
Computed
tomographic findings in a
patient
with
chronic
recurrent
aspiration.
Multifocal, patchy air-space
disease
is
present
bilaterally with a tree-inbud pattern seen in the
periphery of the lungs
where aspirated material
has become inspissated in
bronchioles. Note also the
dilated esophagus with
retained contrast material
within the lumen.

Pneumonia in Children
Differences in response to pulmonary infection in infants and young children,
compared with older children and adults, are probably based on anatomic and
immunologic factors.9,64 Airways are small, soft, and easily collapsible; resultant air
trapping with overinflation can be found in a variety of infections in the first 12 to 18
months of life. In the newborn period, B streptococcal pneumonia causes an
appearance similar to that of hyaline membrane disease. In fetal aspiration syndrome,
rapid roentgenographic changes result as the aspirated material is cleared and
overinflation disappears.
Staphylococcal pneumonia has a very rapid course, with early development (within
hours) of effusion, empyema, and bronchopleural fistula with pyopneumothorax or
lung abscess.90 Pneumatoceles are very common as the pneumonia clears.
Upper-airway infection may be associated with pulmonary disease, so a chest
roentgenogram may be the initial study. When lungs are hypoaerated or edematous,
obstruction due to epiglottitis should be suspected.
It is very important to correlate the roentgen findings with clinical signs and
symptoms. For example, Chlamydia trachomatis causes conjunctivitis in neonates and
may produce pneumonia which is interstitial, scattered, and bilateral and is associated
with overinflation of the lungs. Cough is often the only symptom, so a chest film
showing these findings in a neonate with conjunctivitis should suggest the diagnosis.
113

Klebsiella (Friedlnder's)
Pneumonia
Klebsiella pneumonia is a confluent alveolar type of pneumonia caused
by Klebsiella pneumoniae. The disease occurs most frequently in elderly
and debilitated patients. The onset is usually sudden, and the illness is
often fatal within a few days. It may begin as bronchopneumonia
manifested by patchy areas of opacity, usually in one or both upper
lobes, but spreads rapidly to become confluent. It may involve an entire
lobe. The involved lobe tends to increase in volume, resulting in
convexity of the adjacent interlobar fissure. Extensive destruction of
tissues leads to abscess formation in many of these patients, and the
abscess cavities are typically thin walled, if a wall can be demonstrated
( Fig. 24-7). Often, the confluent pneumonia surrounding the cavity
obscures its actual wall. At times the necrosis is extensive and extremely
large cavitation results when the necrotic material sloughs out. Pleural
effusion is common, and empyema often follows the effusion. In the more
chronic form, the disease tends to be patchier, the cavitation is smaller,
and the lesions may closely simulate those of TB. Pneumatoceles may
occasionally occur during resolution of Klebsiella pneumonia.

Klebsiella pneumonia

A: The disease is extensive, with evidence of

cavitation in which there are masses of dense
necrotic
material.
B:
Ten
days
later,
considerable advance of the disease is evident.

 The diagnosis should be suspected when a rapidly progressing confluent

pneumonia is observed in one or both upper lobes, resulting in increased lung
volume, in which cavitation forms quickly. When the disease progresses more
slowly, it is often less confluent, and its distribution in one or both upper lobes
plus the presence of cavities often leads to a mistaken diagnosis of TB.
Bacteriologic studies are then needed for differentiation. In patients who
survive, a considerable amount of fibrosis may result, leading to contraction of
the lobe with secondary changes in the thorax resulting from the loss of lung
volume. In this respect, the disease may resemble chronic TB.
Enterobacter and Serratia are similar gram-negative bacteria that cause
pneumonia infrequently. The most common of these is Serratia marcescens,
which usually causes either a focal pneumonia or a diffuse process that may
involve several lobes. Pleural effusion is common. Both Enterobacter and
Serratia are usually found in debilitated hospitalized patients, often in
association with other organisms as a cause for pulmonary infection. As an
opportunistic pathogen in immunosuppressed patients, Serratia may produce a
necrotizing bronchopneumonia but usually does not cause a frank lung abscess
.

Rapid progression of gramnegative pneumonia from rightupper-lobe consolidation ( A) to

extensive cavitation (B and C) in
10 days

Staphylococcal
Pneumonia
Pneumonia caused by Staphylococcus aureus may be primary in the lungs or secondary to a primary
staphylococcal infection elsewhere in the body. In the secondary type, there is hematogenous spread of
the organism, whereas in the primary type the pulmonary spread is usually bronchogenic. The disease
usually occurs in debilitated adults and in infants during the first year of life, and recurrent staphylococcal
infections are common in patients who use intravenous drugs and those with AIDS. The onset of the illness
is usually abrupt, with severe prostration. Death may occur within 24 to 48 hours. Because some of the
many areas of involvement occur adjacent to the pleura, it is common to have pleural infection with
empyema and bronchopleural fistula.
In children, the roentgen findings are rather characteristic and consist of dense areas of pulmonary
involvement that may be segmental and local or diffuse. Consolidation rapidly spreads to involve a whole
lobe (confluent bronchopneumonia); bronchi are usually obscured by exudate, so an air bronchogram is not
ordinarily seen. Pleural effusion, empyema, and pneumothorax are common, and pneumatoceles are often
noted. Abscess formation may also occur, and coalescence of small abscesses is frequent. A pneumatocele
is distinguished from an abscess by its thin wall and rapid change in size. The pathogenesis of
pneumatoceles is not known with certainty. The most popular theory hypothesizes that a check-valve
obstruction develops between the lumen of a small bronchus and the adjacent interstitium. Multiple
pneumatoceles may develop, usually in the first week of the disease, and they may become very large.
Accumulation of fluid with airfluid levels is common during the active phase of pneumonia.
Pneumatoceles may persist for months but usually disappear completely ( Fig. 24-9). In adults the findings
are not as characteristic. Pneumothorax and pneumatocele are less common but do occur, and pleural
effusion and empyema are not as common as in children, with the exception of patients with AIDS and
intravenous drug users. Abscesses are slightly more common than in children and tend to coalesce ( Fig.
24-10).
The disease is usually bilateral, may be diffuse and somewhat nodular, but is seldom lobar in distribution.

Staphylococcal pneumonia in
the left lower lobe resulting in
the
formation
of
a
pneumatocele. A: Note the
homogeneous opacity at the
left base, indicating rather
extensive pneumonia. There is
a
radiolucent
area
surmounting a fluid level. The
pulmonary alveolar disease
surrounding the pneumatocele
makes
it
impossible
to
determine the thickness of the
wall. B: The inflammatory
disease has cleared almost
completely, leaving the thinwalled,
cyst-like
pneumatocele. This film was
obtained 1 month after that
shown
in
A.
C:
The

Staphylococcal pneumonia

There is extensive disease in the left

lower lobe, in which numerous small,
rounded, lucent areas represent small
pneumatoceles or abscesses.

 Pleural effusion, often resulting in

empyema, occurs in about one half of the
patients. Rapid change and lack of
correlation between severity of clinical
symptoms and roentgen findings are
often observed. Resolution is usually slow
in both children and adults. When the
disease is hematogenous, septic emboli
may cause multiple small abscesses and
widespread, small foci of pneumonia.

Streptococcus pyogenes
Pneumonia
Pneumonia caused by S. pyogenes (Lancefield group A,
hemolytic streptococcus) usually occurs after such acute
infectious diseases as measles and influenza. This disease is
now rare. It is roentgenographically similar to staphylococcal
pneumonia in the frequency of pleural involvement, including
empyema if antibiotic therapy is not initiated promptly. The
pulmonary involvement has a tendency to be more diffuse
and interstitial in type than in staphylococcal pneumonia, with
fine opacities radiating outward to the periphery from the hila.
The combination of rapidly developing, hazy, nodular opacities
in an acutely ill patient with subsequent cavitation in many of
the areas is highly characteristic of either staphylococcal or
streptococcal pneumonia, with the former more likely. S.
pyogenes infections usually do not cause pneumatoceles.

Tularemic Pneumonia
Tularemia is an infectious disease caused by Francisella tularensis, a small gramnegative bacillus. It is a disease of small animals and may spread to humans directly
from the animals.127 The most common mode of infection is through the skin of
hunters who dress small game. The infection may also be transmitted by means of tick
bites as well as the bites of horse and deer flies. Pulmonary involvement in the form of
pneumonia resulting from this organism is present in approximately 50% of humans
affected. The roentgen findings are not characteristic, but some authors have reported
a high incidence of oval lesions resembling an abscess without cavitation. However,
others have indicated a great variability in pulmonary findings. 91 The infection may
produce unilateral or bilateral pulmonary inflammatory disease, which is usually poorly
circumscribed. Occasionally, the distribution is lobar, resulting in consolidation of an
entire lobe. The infection is commonly a basal one, and there is usually more disease
on one side than the other, so that it is asymmetrical when bilateral. A small amount
of pleural effusion is not uncommon, 26 and hilar lymph-node enlargement is also
present in many instances. The time required for resolution varies widely. In some
patients complete clearing may occur within 7 to 10 days, and in others the disease
may persist for 6 weeks. Because the roentgen picture is not characteristic, the
diagnosis must be confirmed by laboratory methods. The organisms are difficult to
isolate from the sputum, but if the disease is suspected, its presence can be proved by
means of agglutination tests.

Brucellosis Pneumonia
Brucellosis in humans in the United States is usually caused by
Brucella suis. Pulmonary involvement is rare, and symptoms are
usually mild.41,103 The roentgen findings are varied. Strands of
opacity that radiate outward from the hila are often associated
with hilar adenopathy and may be bilateral. Pleural involvement
with effusion is occasionally encountered. In other instances,
widespread miliary disease that resembles miliary
bronchopneumonia is found. Solitary, circumscribed pulmonary
nodules have also been described. The pulmonary roentgen
changes appear quickly but tend to persist for long periods with
very slow resolution. The diagnosis cannot be made on roentgen
examination but must depend on the results of bacteriologic
studies, agglutination, and skin tests. Calcifications in the spleen
that have a typical appearance may be a clue to the diagnosis in
the patient with the appropriate exposure history.

Pertussis Pneumonia
Whooping cough is usually caused by Bordetella pertussis. The
organism may also cause pneumonia, an unusual but not rare
complication. The pulmonary disease begins in the paroxysmal
stage of whooping cough and extends into the resolution phase. It
is usually found in children but may occur in adolescents and
adults.
The pulmonary disease tends to be central, with radiating
parabronchial strands of opacity. The radiographic findings resulting
from this distribution of disease consist of blurring of the cardiac
margins and an irregular appearance termed the shaggy heart
pattern. There may also be some subsegmental areas of
consolidation as well as scattered areas of atelectasis, presumably
caused by mucus plugs, particularly in older children and adults. In
some instances, the pneumonia may be caused by other organisms
complicating whooping cough, a widespread bronchopneumonia.

Pseudomonas Pneumonia
There is an increasing incidence of pneumonia caused by Pseudomonas aeruginosa, a gramnegative bacillus. Cases usually occur among hospitalized patients and are often related to the
use of antibiotics, steroids, and immunosuppressive and cytotoxic drugs. There is evidence that
positive-pressure breathing apparatus, 57 suction and nebulizing devices, and tracheostomies
are major factors in the development of this disease. P. aeruginosa is a water-associated
organism found in many environmental sources, both in the hospital and outside it. 117 The
causative organism is extremely difficult to eradicate once pulmonary disease is established.
Several roentgen patterns of pulmonary involvement have been described: (1) bilateral
pneumonic consolidation, with early patchy, scattered disease progressing and coalescing to
involvement of the major portions of both lungs; (2) extensive bilateral pneumonic
consolidation with abscess formation (abscesses may be multiple and small or few and large);
(3) diffuse nodular or patchy densities with or without abscess formation; and (4) unilateral
pneumonia, similar to the coalescent bilateral pneumonia. Many species of Pseudomonas are
angioinvasive. Pathologic specimens show that bacterial colonies actually invade pulmonary
blood vessels and cause a vasculitis and thrombotic occlusion. This predisposes areas of
Pseudomonas pneumonia to undergo necrotic infarction, and lung cavitation is a prominent
feature of many Pseudomonas infections.29 Therefore, almost any pattern may occur, so the
radiographic findings are not diagnostic ( Fig. 24-11). Pleural effusion may occur, but it is not a
prominent feature of the disease. There is evidence that the presence of P. aeruginosa in the
sputum of patients with chronic lung disease indicates underlying bronchiectasis.

Pseudomonas pneumonia in a patient with chronic

debilitating disease. A: Initial examination reveals
bilateral diffuse disease at the right medial base and in
the left parahilar area. B: One week later, note the masslike opacity in the left midlung and more patchy disease
in the right midlung and medial base. There is nothing
characteristic about the disease pattern, as is often the
case. C: Diffuse hematogenous dissemination in another
patient. Note scattered, poorly defined disease, largely
basal.

 Although most Pseudomonas infections occur in debilitated or hospitalized

patients, they can occur in otherwise healthy persons. Serious, even fatal,
Pseudomonas pneumonias have been associated with use of home and motel
whirlpool spas and jacuzzis, presumably because of inhalation of large numbers
of aerosolized bacteria from contaminated units into the lungs. 68,117
Melioidosis, which is caused by infection with P. pseudomallei, is endemic in the
tropics, chiefly in India, Burma, Sri Lanka, and South America. Since the Vietnam
War, sporadic cases have been reported in the United States, chiefly in Vietnam
veterans. 19 The infection may be acute or chronic. The acute form is more
common and is characterized by indistinct nodular disease that is often widely
scattered but tends to involve the upper lobes. The nodules coalesce and
cavitate in a high percentage of cases. The chronic form simulates pulmonary TB,
because the nodules often involve the upper lobes and frequently cavitate. Hilar
adenopathy is uncommon, and pleural effusion is rare.
Occasionally, pulmonary cavitation appears acutely years after the initial
infection, so it should be suspected when a parenchymal cavity appears in an
apparently healthy patient who was in an endemic area some years earlier.

Anaerobic Bacterial Pneumonias

Several anaerobic organisms may cause pulmonary infection. They include,
among others, Bacteroides fragilis, Bacteroides melaninogenicus, and
Bacteroides oralis; members of the genera Fusobacterium, Clostridium, and
Eubacterium; and the gram-positive cocci of the genera Peptostreptococcus and
Peptococcus. Most of the infections are caused by several organisms, because
many are caused by aspiration of oral secretions, particularly in patients with
poor oral hygiene. They may also occur in diabetic patients, those with malignant
disease, and immunosuppressed patients. An alveolar type of pneumonia, which
may be extensive, is usually produced. The right lower lobe is the most common
site, but frequently more than one lobe is involved. About one half of patients
have pulmonary disease only, about one fourth have pleural and parenchymal
disease, and the remainder have only the pleura involved, usually with
empyema. Abscess formation and necrotizing pneumonia are common
complications. Abscess occurs in more than 50% of patients with pulmonary
disease. Bronchopleural fistula may also complicate the disease.
Anaerobic bacteria therefore are a prominent cause of aspiration pneumonia,
lung abscess, necrotizing pneumonia, and empyema. The mortality rate is high in
these patients, many of whom have depressed immune responses or
leukopenia.13

Other Bacterial Pneumonias

Pneumonia caused by infection with Proteus vulgaris is largely basal, may be alveolar or lobular in
distribution, and tends to produce cavitation. It may cause a decrease in volume of the involved lung. Rarely,
Escherichia coli causes pneumonia, which is usually multilobar and basal. Pneumatoceles are occasionally
seen in this infection, and the alveolar pneumonia caused by this organism rarely results in massive
cavitation. Pleural effusion is common.
Pneumonic involvement may occur in typhoid fever, usually as a bronchopneumonia with cavitation, pleural
effusion, or empyema. Salmonella organisms other than Salmonella typhosa may produce a similar pattern in
the lung. An acute miliary pattern has also been described in salmonella bacteremia. 42 Hemophilus
influenzae, type B, is a rare cause of pneumonia9 that is being seen increasingly in HIV-positive patients as a
cause of pneumonia.
In adults, these infections appear as acute lobular lower-lobe pneumonia or as a more confluent lobar
alveolar process. The latter is somewhat more common.
Pneumatoceles are rare but have been reported. Patients with alcoholism, who are immunocompromised, or
who are undergoing chemotherapy are at risk. In infants, pleural effusion and empyema are common in
addition to extensive alveolar disease. The latter may be a patchy, segmental type of density, but a variety
of manifestations have been described, including reticular or linear, nodular, reticulonodular, ground-glass,
and honeycomb patterns. Pleural effusion is fairly common and may be complicated by empyema. Cavitation
is rare; roentgenographic findings clear slowly.
Pulmonary involvement also occurs in patients with anthrax or bubonic plague. In anthrax pneumonia, there
is often substantial mediastinal lymph node enlargement, pleural effusion, and sometimes intrapulmonary
hemorrhage in addition to extensive pulmonary disease. Plague can often involve the lung. 5 In secondary
pneumonic plague, bilateral small densities are the most common early manifestation. The disease may
spread to involve much of the lungs with a dense alveolar process, which is often fatal. Rarely, the pattern is
that of bilateral extensive mottled densities, which resemble the pattern of ARDS. This pattern reflects
intravascular coagulopathy in some instances.

Legionnaires' Disease
Legionnaires' disease, which affected almost 200 people at the Legionnaires' Convention in Philadelphia in
July 1976, is caused by the aerobic, gram-negative bacillus Legionella pneumophila.27 Since this original
description, 34 Legionella species and 52 serogroups have been isolated, with about half proving pathogenic
to humans. The bacteria is associated with water reservoirs, including air-conditioning cooling towers. 116
Clinically, the acute disease is characterized by a high fever, chills, and a nonproductive cough, often
associated with chest pain, malaise, muscle and abdominal pain, headaches, and gastrointestinal symptoms.
Hyponatremia and elevated creatine phosphokinase are two abnormal laboratory results that can occur with
Legionnaires' disease but are not often present in patients with other community-acquired pneumonias.116
Since the outbreak in Philadelphia, many sporadic and local outbreaks throughout the United States have
been reported.
Predisposing factors include smoking, alcoholism, diabetes, heart disease, and immunosuppression.
Roentgen findings are largely those of an alveolar pneumonic process that is bilateral in about one half of the
reported cases ( Fig. 24-12). There tends to be lower-lobe predominance. The alveolar disease may have a
lobar or lobular distribution. At times, the alveolar process appears as a large, very poorly marginated,
generally round or oval opacity. Some of these are central and some peripheral; they may be unilateral or
bilateral. The round lesions appear to be somewhat more common than any other roentgen manifestation.
The round, mass-like lesions often progress rapidly to involve an entire lobe. Early in the disease there may
be patchy, ill-defined opacities that in many cases progress to a lobar pattern. One patient has been reported
in whom there was virtually universal involvement of both lungs by an alveolar process in which air
bronchograms were very prominent. Cavitation, presumably a result of necrotizing pneumonia, has been
reported in several patients, most of whom were immunosuppressed. One patient has been reported in
whom pneumatocele formation and spontaneous pneumothorax were manifest.
Pleural effusion may occur, but its incidence is difficult to evaluate because many of the patients have
complicating renal or cardiovascular disease. Resolution is usually slow and lags behind clinical
improvement. An interstitial pattern may appear during resolution.

Legionella pneumonia in a patient with acquired immunodeficiency syndrome. A: Initial film

shows bilateral upper-lobe disease, which appears to present a mixed interstitial and alveolar
pattern. B: Two and one-half weeks later, there is extensive bilateral disease which appears to
be in a largely alveolar pattern. This disease is more diffuse and less mass-like than the
original descriptions.

 It is evident that there is a wide variety of roentgen patterns in this disease,

so the diagnosis cannot be made on the basis of chest roentgenograms.
However, the disease should be suspected in a patient with atypical
pneumonia in whom roentgenograms show unilateral or bilateral, large,
poorly marginated, rounded alveolar opacities that progress rapidly to involve
one or more entire lobes.
The Pittsburgh pneumonia agent (Tatlockia micdadei, Legionella micdadei)
was described in 1979. It is a gram-negative, weakly acid-fast bacillus that
appears to be identical to the Tatlock organism isolated 37 years earlier. It has
been recognized as a disease seen mainly in renal transplantation patients
and others treated with high-dose corticosteroid therapy. However, it has also
been reported 94 in patients who were not immunosuppressed. Radiographic
findings are those of an alveolar type of pneumonia, usually in one lobe,
either segmental or subsegmental and nodular in appearance. In the
compromised patient, it spreads very rapidly and occasionally cavitates.
Pleural effusion is found in about 30% of patients. The organism is similar to L.
pneumophila, and the two diseases are found simultaneously in a few
patients. The diagnosis is made by lung biopsy.

Hospital-Acquired
(Nosocomial) Pneumonias
Hospital-acquired pneumonias are important because the impaired resistance
of the hospital patients renders them very susceptible to gram-negative bacilli
such as P. aeruginosa, E. coli, and other Enterobacter species. Outbreaks of
Staphylococcus, Klebsiella, Proteus, and other pneumonias have also been
reported.
Furthermore, the wide use of antibiotics has resulted in resistant pathogens
that may also cause pneumonia. The lungs are involved in 10% to 30% of
infections acquired in hospitals. In this patient population, mortality may be
very high and every precaution must be taken to avoid contamination of
respiratory therapy equipment, anesthesia machines, air-conditioners, and
other devices used in patient care. Pseudomonas infection is particularly
common in this group of patients, is very difficult to treat, and has a high
mortality rate despite treatment with various combinations of antibiotics.
Nosocomial pneumonia should be considered when a hospitalized patient
develops leukocytosis, cough, or fever. In this situation, any new or increasing
pulmonary opacity may represent pneumonia. There are no specific patterns
for the various organisms involved, so the radiologist's role is to note the
disease and suggest the possibility of pneumonia.

Viral, Mycoplasmal, and

Rickettsial Pneumonias
Mycoplasmal Pneumonia
Mycoplasma pneumoniae (the Eaton agent) pneumonia is responsible for a significant percentage
of primary atypical pneumonia in children and young adults (15% to 20% or more). It probably
accounts for almost 50% of pneumonias found in children younger than 16 years of age. The
remainder of patients with primary pneumonia have disease caused by adenovirus, parainfluenza
virus, respiratory syncytial virus, and probably other viruses. In many patients, the cause is not
determined. Cold agglutinins are found in the serum of 50% to 60% of patients with Mycoplasma
pneumonia. A titer of 1:32 or higher is considered positive and is usually found 10 to 14 days after
onset of the symptoms. A high titer is usually present. Mycoplasmal pneumonia tends to occur in
epidemics, as well as sporadically, so it is difficult to obtain meaningful figures as to relative
frequency. The disease usually occurs in young, healthy adults. It is acute, mild, and self-limited in
most instances but may be severe with widespread pulmonary disease. Occasional fatalities have
been reported. The inflammatory exudate is sometimes more interstitial than in the bacterial
pneumonias, but alveolar exudate, which contains fewer cells and more fluid than in the bacterial
type, is also present. The onset of symptoms is gradual, and there is often a delay in the
appearance of visible pulmonary density on roentgen examination for 2 or 3 days. Putman and
colleagues 108 described two groups of patients with different clinical and radiographic findings.
One group with acute chest pain, cough, and fever developed segmental or lobar air-space
disease. The other group had a more chronic course, were afebrile, and had no cough or chest
pain. They developed interstitial changes and a reticulonodular or mixed pattern of focal air-space
and interstitial disease. Others have noted less relation between symptoms and anatomic
distribution.

 Roentgen findings reflect the anatomic changes. Recognizable forms can be

divided into several types:
1. Peribronchial or interstitial type. The findings in the peribronchial type consist of
streaky densities extending outward from the hilum following the pattern of the
vascular markings, limited to a single segment or affecting one or several lobes.
Alveolar exudate may produce scattered patchy density as well as the linear
shadows.
2. Bronchopneumonic type. The roentgen findings are similar to those described for
bronchopneumonia and may be just as widespread. Opacities that are usually poorly
defined and scattered may be noted in any lobe or segment and may be bilateral.
3. Segmental and lobar types. The findings are those of homogeneous density
representing consolidation in a segment, several segments, or a lobe. Single-lobe
involvement occurs in almost 50% of patients. Air bronchograms may be present.
The appearance of the consolidation is similar to that found in S. pneumoniae lobar
pneumonia. Pleural effusion occurs in about 20% of patients with this type of disease
and is rare in the interstitial type.
4. Diffuse type. A bilateral reticulonodular pattern throughout both lungs. Pleural
effusion is rare.

 One or more of these gross anatomic types of the disease

may be present in a single patient. There is a tendency for the
disease to clear in one area and spread in another, often in
the opposite lung. Atelectasis may be produced by bronchial
obstruction and is frequently lobular and focal in type.
Occasionally, a pneumatocele may result from check-valve
obstruction and must be differentiated from lung abscess (see
Fig. 24-7). Resolution is usually slow, and it is common to see
persistent pulmonary lesions for a week or longer after the
clinical findings have disappeared. Occasionally, the delay is
considerably greater. Mycoplasmal pneumonia cannot be
differentiated from viral infections of the lung, and when the
distribution is segmental or lobar it is similar to bacterial
pneumonia ( Fig. 24-13, Fig. 24-14 Fig. 24-15).

Viral pneumonia

A: Extensive interstitial disease is seen throughout the

entire right lung, with similar but much less marked change
on the left. B: Diffuse involvement, which appears to be
mainly interstitial, is confined largely to the right upper lobe
in another patient.

Viral pneumonia

In these two patients, the disease is largely

alveolar in type, being rather diffuse in the
patient shown in A and localized into an irregular,
mass-like lesion in the patient shown in B.

Mycoplasmal pneumonia

A: The air bronchogram denotes alveolar disease,

but there also appears to be some interstitial
change in the upper central lung. B: Alveolar
pneumonia, which is probably subsegmental, is
noted in the left lower lobe.

 In the differential diagnosis, there are findings that help to

differentiate mycoplasmal from bacterial pneumonia. They
consist of the lack of pleural involvement, manifested by
absence of elevation of the diaphragm and absence of
pleural fluid in most cases. The delay in appearance of
pulmonary disease after clinical onset is also helpful. The
tendency to clear in one area and spread in another is
more common in this disease than in bacterial pneumonia.
Bilateral involvement is probably more common than in
bacterial pneumonias, with disease often in one lower lobe
and the opposite upper or middle lobe. However, because
the roentgen pattern may vary widely, the diagnosis must
be substantiated by clinical and laboratory findings ( Fig.
24-16).

Viral pneumonia simulating minimal tuberculosis. A: Note the disease in the

right subclavicular area. B: Close-up view shows the disease in the first
anterior interspace. C: Roentgenogram of the same area shown in B, obtained
2 weeks later, shows complete clearing of the disease.

Adenovirus Pneumonia
There are 28 types of the adenovirus, which is a common cause of
upper respiratory disease and may cause pneumonia, often in
epidemics. The disease is usually more severe in infants and young
children than in adults. The most common roentgenographic
pattern is that of a widely scattered patchy or confluent disease,
usually in a peribronchial distribution. Slow resolution is usually
noted, with residual bronchiectasis in some children and obliterative
bronchiolitis and other chronic lung disease in others. This virus
also causes acute bronchiolitis with overinflation in infants and can
cause unilateral hyperlucent lung (Swyer-James syndrome).
Bronchiolitis can also be caused by other viruses such as the
respiratory syncytial virus, rhinovirus, influenza virus, and
parainfluenza virus, usually in children. It is unusual in adults and is
rarely diagnosed. Although pulmonary involvement may be
extensive, the acute illness may not be severe, particularly in
adults.

Other Viral Pneumonias

Several viruses are capable of causing pneumonia, often in epidemics. 24 A number of new viral diseases, including Ebola fever
and Hantavirus pulmonary syndrome, have emerged in recent years as life-threatening epidemics. 14 The roentgenographic
findings of most viral pneumonias are similar to those described for mycoplasmal pneumonia, so the cause cannot be established
on the basis of these findings alone. In some epidemics, the pericardium is involved, leading to effusion, often associated with
pleural effusion as well. Often the virus is not definitely identified in these patients and the diagnosis is based on clinical findings.
The disease usually is not as prolonged or severe as mycoplasmal pneumonia.
Epidemic influenza, which is a viral disease, may be associated with virus infection of the pulmonary parenchyma in addition to
involvement of the tracheobronchial tree. Roentgen signs are variable, with findings often bilateral and extensive. Especially in
severe epidemics of the past, the pneumonia was often of the interstitial type with hazy, strand-like densities radiating outward
from the hila. These result in a coarse appearance of the bronchovascular pattern and irregular hilar thickening.
In other patients, segmental or lobar consolidation may be present; it may be bilateral. A diffuse, patchy pattern resembling
pulmonary edema has also been described. Pleural effusion is rare in uncomplicated influenza pneumonia. The diagnosis is often
made from clinical findings during an epidemic. The roentgen changes are then largely confirmatory, but radiographic
examination is useful to observe the course of the pulmonary parenchymal disease. A complicating staphylococcal pneumonia
may also occur, particularly in epidemics in which influenza is severe. Most fatalities are caused by this complication.
Herpes simplex pneumonia may occur in neonates and immunocompromised hosts. It is a severe, often fatal disease in
neonates, with an initial interstitial pattern progressing to coalescent air-space densities and a diffuse alveolar white-out of
both lungs in the fatal cases. The pathology is that of a necrotizing hemorrhagic pneumonia. The disease is usually widely
disseminated in these neonates.
Pneumonia associated with chickenpox (varicella) is believed by some to be viral in origin and has been reported occasionally. It
usually occurs in adults with severe chickenpox. Roentgen findings consist of widespread, poorly defined, patchy or nodular
densities associated with an increase in parahilar markings and occasionally enlargement of the hilar nodes ( Fig. 24-17).
Densities are most marked in the parahilar areas and at the bases. Individual nodules are generally round but are poorly defined
peripherally. There is often considerable change in the roentgen findings from day to day, because the densities are transitory.
Clearing is usually slow, however. In patients with fatal disease, pulmonary involvement may be virtually total, with little if any
visible aerated lung. In rare instances, scattered small calcifications result from varicella pneumonia in adults. No hilar node
calcification is observed. It is entirely possible for bacterial pneumonia to appear in patients with these various viral diseases and
there is no way to differentiate the cause on chest radiographs.

Varicella Pneumonia
Varicella
pneumonia in an
adult. Soft,
rounded nodular
opacities are
noted bilaterally.

 Measles (rubeola) is occasionally associated with pneumonia caused by the virus. 110 Pneumonia caused by other
organisms sometimes complicates measles, however, so roentgen differentiation is not possible. The measles virus
causes reticuloendothelial involvement resulting in hilar and mediastinal adenopathy. The virus may also involve the
lung to produce an interstitial process that is manifested as a widespread reticular type of reaction, with predilection for
the bases.
Consolidation of lung with varying degrees of atelectasis most probably represents a complicating bacterial pneumonia.
Atypical measles pneumonia occurs in adolescents and young adults after previous incomplete immunity conferred
by killed rubeola virus vaccine. It is probably a hypersensitivity response in incompletely immunized patients. The
pneumonia is usually segmental and bilateral but may involve most or all of a lobe. Other patterns include round
pneumonia, diffuse perihilar opacity, and multiple nodules. Pleural effusion and hilar adenopathy occur in about one
third of patients. Usually the patients have the skin eruption of measles. The acute pneumonia usually clears promptly,
but rarely a nodule persists for 1 to 2 years. 83
Pneumonic involvement may occur with several other viral diseases, including smallpox, lymphocytic choriomeningitis,
and cytoplasmic inclusion disease in infants and children. There is nothing characteristic about the roentgen
appearance of the pneumonia associated with these diseases except that the pneumonia is usually bilateral and often
extensive. Cytomegalovirus infection is the most common viral infection in immunosuppressed patients. In patients
having cytomegalovirus disease, nodules have been reported involving the outer one third of the lungs. Lung biopsy
may be necessary to establish the diagnosis.
Hantavirus caused an outbreak of a new fatal pneumonia in young, otherwise healthy persons living in the
southwestern United States in 1993. Since then, an increasing number of cases have been identified outside of that
area as well. The virus is spread by rodents; inhalation of aerosolized, virus-infected rodent droppings is the mode of
transmission to humans. Patients present with a prodrome of fever and flu-like symptoms, followed by cough,
increasing dyspnea, and rapid progression to fulminant pulmonary failure, which is often fatal. 58,61 The chest film
often shows bilateral, interstitial edema with rapid progression to a picture of noncardiogenic pulmonary edema with
bilateral air-space disease and normal heart size. Widespread increased capillary permeability within the lungs is
believed to be the cause of the roentgenographic findings and rapid development of pulmonary edema in infected
patients. Copious secretions may be noted on bronchoscopy or on suctioning.58 Pleural effusions are common.61

Psittacosis (Ornithosis)
Psittacosis, or ornithosis, caused by Chlamydia psittaci, is
primarily a disease of birds and is transmitted to humans by
members of the parrot family. 125 It is also found in other
domesticated and wild birds and may be transmitted to
humans by them. The disease may be unilateral or bilateral,
focal or multifocal, resembling lobular pneumonia. This results
in a roentgen pattern of patchy consolidation that may be
relatively focal or bilateral and widely scattered. A reticular
pattern (interstitial) has also been reported. Enlargement of
hilar nodes may also be present. Pleural involvement is
uncommon. The roentgen changes tend to persist for a long
time (6 to 9 weeks) after the initial symptoms. The diagnosis is
confirmed by serologic and bacteriologic studies but can be
suspected when this type of disease is seen in a patient who
has had contact with birds.

Chlamydia trachomatis
Pneumonia
There have been several reports on the radiographic findings in C.
trachomatis pneumonia in infants younger than 6 months of age,
and this organism has been reported as the causative agent in a
distinctive pneumonia in this group. Radkowski and associates 113
reported on 125 patients observed over a period of 3 years.
Although the x-ray findings are not diagnostic, most patients have
hyperinflation plus a variety of patterns of bilateral disease,
including relatively minimal interstitial disease, areas of atelectasis,
patchy coalescent pneumonia involving small volumes of lung, and
rare pleural effusion. 126 The clinical signs and symptoms are
relatively few, so the chest findings on radiography are those of
more disease than would be expected. The infants are afebrile but
have a cough, conjunctivitis, and elevated serum immunoglobulins.
In adults there are streaky opacities, usually bilateral, with
associated atelectasis but rarely pneumonic consolidation. 30

Rickettsial Pneumonias
Q Fever. Q fever is caused by a rickettsia, an intracellular parasite considered to be
intermediate between bacteria and viruses. The causative organism is Coxiella
burnetii. The roentgen findings consist of a subsegmental, segmental, or lobar
consolidation varying from a patchy nonhomogeneous shadow to frank air-space
opacity in the area of involvement. Hilar node involvement and small focal lesions are
uncommon. There appears to be a difference between sporadic and epidemic
disease.41 Round pneumonia, sometimes multiple, is common in the epidemic group
but less so in sporadic cases. Pleural involvement is rare in epidemic disease and
occurs in approximately one third of the sporadic cases. This is manifested by a small
amount of pleural fluid. The roentgen findings usually appear within 48 hours of onset
of disease and resolve rather slowly, so that the pulmonary consolidation persists
longer than in pneumococcal pneumonia. This disease does not exhibit the migratory
type of change often found in viral pneumonia. As in other pneumonias, the diagnosis
depends on correlation of clinical, roentgen, and serologic findings.
Other Rickettsial Pneumonias. Pulmonary involvement has been reported
occasionally in patients with other rickettsial diseases such as Rocky Mountain
spotted fever and typhus, when severe. The roentgen findings are not characteristic
in these diseases, but the opacities usually are scattered and produce disseminated
shadows on the chest roentgenogram.

Other Infections: Lung Abscess

When an acute suppurative pulmonary infectious process breaks down to form a cavity, regardless of size, it is termed lung abscess. Most
lung abscesses are bronchogenic in origin and result from aspiration of foreign material after dental operations, surgery of the respiratory
tract and elsewhere, and various conditions that produce unconsciousness. This type of abscess may also be secondary to stasis of
secretions from various causes (e.g., bronchogenic carcinoma) or other endobronchial obstructions that result in incomplete drainage of a
bronchus. As indicated, anaerobic organisms are often the cause of lung abscess. Hematogenous lung abscess, which is usually produced
by staphylococcus and occasionally by streptococcus, has been discussed in a previous section, as has the abscess formation in
pneumonia produced by Klebsiella. Cavitation occurs in approximately 5% of patients with pulmonary infarction and, when infected, an
abscess is formed.
Because lung abscess is, in many instances, the result of aspiration of foreign material, it is usually found in areas of the lung that are
dependent at the time of aspiration. The posterior segment of the upper lobe is the most common site, and the right side is affected more
than the left. The next most common sites are the superior segments of the lower lobes, because these segments are dependent when
the patient is supine. The basal segments of the lower lobes are also commonly involved, and abscess can occur in any segment of any
lobe. The lesion is peripheral in relation to the bronchopulmonary segment involved, but on the frontal roentgenogram it may project in a
central position. The pleura adjacent to the abscess is usually involved, so there may be pleural effusion.
The early roentgen finding is consolidation that produces an opacity which is usually confined to one pulmonary segment.
Characteristically, the lesion has an opaque center with a hazy and poorly defined periphery and is often roughly spherical in shape.
When bronchial communication is established, the fluid contents of the cavity are replaced, at least in part, by air, and the radiolucent
abscess cavity appears within the area of disease. It is usually incompletely drained, so that an airfluid level can be outlined within it. In
these cases the fluid produces, in the dependent portion, homogeneous opacity that blends with the wall of the cavity. Drainage of the
abscess may vary, so that at times it may contain more or less air. When the necrotic lung tissue has not sloughed completely, it is
common to observe a crescent-shaped radiolucency caused by air in the superior aspect of the partially formed cavity. In some patients,
several small cavities may appear within the area and remain as separate lesions or coalesce to form one or more larger cavities. These
may be well outlined on the routine frontal and lateral roentgenogram, but small cavities can be hidden by the surrounding pneumonic
consolidation. When cavitation is suspected, computed tomography (CT) may be indicated, because it can reveal lesions not seen on
plain films. CT also aids in localizing and in defining the inner and outer walls of the abscess cavity and may identify complications such
as rupture of the cavity into a bronchus or into the pleural space ( Fig. 24-18). In acute lung abscess the outer wall is usually poorly
defined. As the abscess becomes more chronic, its wall thickens and the external surface is more sharply marginated. Complications are
much less common now than before the use of antibacterial drugs, but empyema and spread of the infection locally or by aspiration of
pus from the abscess into a more dependent portion of the lung may occur. CT occasionally may be necessary to differentiate lung
abscess from empyema and may also be useful to guide percutaneous catheter drainage.

Acute lung abscess

A: Note the irregular radiolucency in the right subclavicular area, in which there is a fluid level. There is a smaller
cavity in the plane of the third anterior rib. B: Tomogram of the upper cavity, which lies posteriorly. The wall is
difficult to define, and a considerable amount of inflammatory disease is present adjacent to the cavity. C: The
smaller cavity is faintly defined on this tomogram. Its medial wall is visualized, whereas the inflammatory disease
laterally produces homogeneous density, making the wall indistinct.

 Differential diagnosis depends on the stage of disease when the

roentgenogram is obtained. In the early stage, before excavation and
communication with a bronchus have occurred, the process cannot be
differentiated from that of a segmental pneumonia. However, excavation
usually occurs early, and the abscess cavity can then be seen on the
roentgenogram if the examination is made with the patient upright. The
clinical findings of cough with profuse, foul-smelling sputum shortly after the
onset of the acute process strongly suggest lung abscess. If the cavity is not
visible on a plain film, CT is indicated. Chronic lung abscess must be
differentiated from cavitary TB, the fungal infections that produce
cavitation, infected lung cyst, and bronchogenic carcinoma in which the
central portion of the lesion has sloughed. This differentiation can be very
difficult to make roentgenographically, and examination of the sputum for
bacteria and fungi along with appropriate cultures is used to confirm the
diagnosis. Cytologic study of the sputum and bronchial aspirates is also
indicated in patients with chronic abscesses, particularly in smokers older
than 40 years of age, because of the high incidence of bronchogenic
carcinoma.

Middle Lobe Syndrome

The term middle lobe syndrome, commonly used in the past, is not used frequently now. It refers to recurrent
pneumonitis and atelectasis in the middle lobe caused by present or previous obstruction of the bronchus to this
lobe. 31 The middle lobe bronchus arises approximately 2 cm below the origin of the upper lobe bronchus and is
relatively pliable, and there are nodes adjacent to it that may produce compression of the bronchus when they
become enlarged. When compression is sufficient to cause partial obstruction, infection can result. The
obstruction may persist or decrease, leading to atelectasis, bronchiectasis, and chronic pneumonitis or to
temporary resolution of the process. Endobronchial disease at the site of the lymph-node compression may result
in gradually increasing stenosis of the middle lobe bronchus. The roentgen findings in the lung are somewhat
varied, depending on the relative amount of pneumonitis and atelectasis. The lobe is usually decreased in size.
This results in downward displacement of the secondary interlobar fissure and an increase in opacity below and
lateral to the right hilum. The opacity is sometimes difficult to see in the posteroanterior roentgenogram,
although it may cause blurring of the right cardiac margin. It usually can be readily outlined on the lateral film.
Then the middle lobe is clearly defined as a wedge-shaped or triangular area of opacity sharply bounded above
and below by normally aerated lung. The apex of the triangle is at the hilum and the base is at the anterior
inferior thoracic wall. When the lobe is not clearly defined in either projection, it may be seen in an
anteroposterior lordotic view. When bronchiectasis is marked, the dilated bronchi may be visible as air-filled
tubular structures within the consolidated lung. The hilar nodes producing the obstruction may contain calcium.
The relationship of these nodes to the middle lobe bronchus can be determined accurately by means of CT.
Collateral ventilation of the middle lobe appears to be relatively ineffective, compared with that of the other
lobes. This may account for the persistent collapse of the middle lobe in this syndrome.
Because bronchogenic carcinoma can cause similar findings, bronchoscopy, with biopsy or even surgical
exploration, may be required to make the diagnosis in this type of disease (Fig. 24-19 and Fig. 24-20).
Surgical removal is the usual treatment, because the bronchial changes are generally irreversible by the time the
syndrome is recognized. Furthermore, there is a high incidence of bronchogenic carcinoma in patients with
recurrent or persistent middle lobe infection and atelectasis.

Middle lobe syndrome

A: Note the contracted middle lobe below the right hilum, which obscures the central portion of the
right atrial silhouette. B: The lateral view shows the contracted middle lobe (arrows). C: The
bronchogram shows obstruction (arrow) of the middle-lobe bronchus. The upper- and lower-lobe
bronchi are partially filled.

Acute pneumonia in the right

middle lobe. A: Hazy
alveolar disease below the
right hilum at the medial
base blurs the right cardiac
margin in this area. B: In the
lateral view, the disease is
clearly defined. It lies in the
right middle lobe.

Pulmonary Cystic Fibrosis

(Mucoviscidosis)
Cystic fibrosis is the term used to describe the generalized process of which fibrocystic disease of the pancreas is the most
commonly recognized finding. It is a congenital disease, transmitted as an autosomal recessive trait, in which there is an
abnormality involving the salivary, mucous, and sweat glands. There also may be an abnormality of mucociliary transport.
Sodium and chloride levels in the sweat are elevated, so the diagnosis can be confirmed by a positive sweat test (a finding
of more than 50 mEq of chloride per liter of sweat) and by demonstration of decreased amounts of pancreatic enzymes in
duodenal contents. This disease is discussed here because a major pulmonary manifestation is one of repeated airway and
parenchymal infections. Thick, tenacious mucus tends to obstruct the smaller airways.
Pulmonary manifestations vary in degree but are almost invariably present if the child lives long enough to develop them.
The earliest roentgen change in fibrocystic disease is hyperinflation, which is diffuse and symmetrical. 59 This is often
difficult to recognize in children, but films exposed in inspiration and expiration may indicate the distended state of the
lungs. The degree of obstruction tends to increase to a different extent in various segments, so that small areas of opacity
resulting from focal atelectasis are visible as the disease progresses. These patients experience repeated pulmonary
infection, so findings of pneumonia are superimposed. The infection is usually widespread and peribronchial in distribution,
which leads to a rather irregular, stringy accentuation of peribronchial markings extending outward from the hila on both
sides. This is often associated with areas of poorly defined, hazy opacity caused by
focal areas of pneumonitis. Segmental or lobar collapse may also occur, and the repeated infection leads to a considerable
amount of fibrosis and often to bronchiectasis. Bronchial walls are thickened. This is manifested by the presence of parallel
lines, which represent bronchial walls seen in profile, or thick circles when the thickened bronchial walls are viewed in crosssection. When bronchiectasis is severe, cyst-like structures are visible, usually in the central and upper lungs.
The fibrosis and inflammatory disease produce irregular stringy and patchy shadows. The lung between the consolidated
areas is emphysematous, giving a characteristic roentgenographic picture in far advanced disease ( Fig. 24-21). It is often
possible to suspect the presence of cystic fibrosis early in the disease when hyperinflation, which may often be associated
with small areas of focal atelectasis that are somewhat irregular in distribution, is noted in the infant. Allergic
bronchopulmonary aspergillosis (ABPA), to which patients with cystic fibrosis are susceptible, 70 may be a complicating
factor and is said to be present in 10% of patients. It is probably an important factor in clinical deterioration when it
complicates cystic fibrosis. ABPA is discussed in the section on fungal chest infections.

Cystic
fibrosis
of
the
pancreas
with
chronic
pulmonary disease. There
is extensive involvement
throughout
both
lungs.
Rounded
and
oval
radiolucencies
represent
thick-walled bronchi, some
of
which
are
dilated,
indicating bronchiectasis.
There also is evidence of
some
overinflation,
bilateral hilar adenopathy,
and
patchy
alveolar
disease.

 An increasing number of patients live into adult life, and in these young adults
there is often a rather characteristic radiographic appearance. The disease
usually involves the upper lobes with a combination of patchy, linear, and
nodular densities interspersed with radiolucent areas. In one study
bronchiectasis was observed in 90%; hyperinflation in 76%, particularly in the
lower lobes; and cyst-like air spaces in 24%. 36 There was an increase in hilar
size in 74%. Parenchymal disease was more prominent in the upper and
central lung in 70% ( Fig. 24-22); in the remainder, involvement was general.
Mucus plugs with atelectasis were observed mainly in the upper lobes. In this
study, 30 of 39 patients observed for 1 year or longer showed progression of
the pulmonary disease on chest films. In chronic cases, architectural
distortion develops, with upper-lobe hilar retraction. Rarely, lung abscess may
develop. Hypertrophic pulmonary osteoarthropathy has been reported in
adults with cystic fibrosis. Chronic obstructive pulmonary disease (COPD) is a
major cause of disability in adults with cystic fibrosis. Infections with S. aureus
or P. aeruginosa and cor pulmonale are common causes of death. Adult
patients with end-stage cystic fibrosis are now being treated successfully with
bilateral lung transplantation.

Cystic fibrosis in the adult.

A: In this 28-year-old with
cystic fibrosis who is not
acutely ill, there is upperlobe
predominance,
particularly on the right,
but disease is rather
general. B: Nine months
later, much of the acute
disease has cleared, but
thick-walled,
dilated
bronchi are more clearly
defined; upper and central
predominance is again
noted.

Chronic Granulomatous Disease

of Childhood

Chronic
granulomatous
disease of childhood is
another
genetically
determined
disorder
in
which pulmonary infections
begin early in life and
persist
or
recur
at
intervals.131
Their
leukocytes
phagocytize
bacteria normally but do not
destroy them properly. Lobar
and lobular pneumonia may
occur in these patients,
complicated by lung abscess
and
empyema.
The
organisms usually involved
are staphylococci, Klebsiella,
E. coli, S. marcescens,
Nocardia, and fungi (see Fig.
24-48).
The major features of the
infections
are
hilar
adenopathy and recurrent
pneumonia,
which
often
does not clear completely
and may go on to abscess
formation. In some patients,
the
pneumonia
resolves

Nocardia infection complicating chronic

granulomatous
disease
of
childhood.
Computed
tomogram
shows
multiple
cavitary masses and nodules caused by
disseminated infection.

PULMONARY TUBERCULOSIS:
General Considerations

The incidence of pulmonary TB in the United States decreased from 53 cases per 100,000 in 1953 to 9.4 cases per 100,000 in 1984.
123,129,129A After 1984, this steady decline in the incidence of the disease stopped, and in 1986 there was a 2.6% increase in
reported cases that persisted through 1988. Increasing numbers of cases were being reported in patients with HIV infection, persons
immigrating from countries were TB is endemic, the homeless, the jobless, intravenous drug users, prison inmates, and residents of
nursing homes. These factors, combined with unsupervised and inadequate or noncompliant drug therapy, have led to a resurgence
of multiple-drug-resistant cases as well. 17,98,123,129A These ominous trends stimulated renewed efforts in this country to curb the
infection. New federal funding for TB control clinics to improve case findings and reinstitute the practice of direct observation of
patient treatment appears to have reversed the trend. 123 Overall, new cases of TB in this country decreased to 8.7 per 100,000 in
1995. Nevertheless, incidence rates are much higher in some HIV-infected populations on the east coast. 85,123 Worldwide, the
epidemic of TB goes virtually unabated, with an estimated 7.6 million new cases occurring in developing countries each year. As
many as 3 million people die annually from TB worldwide. 20,123 Therefore, on all fronts, the disease is still of considerable social
and economic importance.
Mycobacterium tuberculosis is an aerobic bacillus that stains acid-fast red with carbol-fuchsin. 35 Most infections occur when
aerosolized droplets containing the organism are inhaled into the lungs and deposited in the middle and lower lobes. 35 An initial
focus of infection develops in the lung and subsequently spreads to regional lymph nodes. Further dissemination occurs via
lymphohematogenous routes to other parts of the lungs, especially lung apices, and to extrapulmonary sites.
The tubercle bacillus injures the tissues, resulting in an alveolar exudate termed tuberculous pneumonia. The disease may advance
rapidly and cause a poorly defined pulmonary shadow of varying size and density. This is usually homogeneous when the lesion is
small. If the process is halted by means of antibacterial drugs before caseation necrosis occurs, complete clearing of the process can
occur. A chest roentgenogram does not permit a positive diagnosis of exudative TB, but the findings may be typical enough that the
diagnosis of an exudative type of lesion can be suggested. Subsequent complete clearing then tends to substantiate the impression.
In the majority of cases, however, primary TB remains clinically silent. Host defenses temporarily contain the infection by forming
granulomas or tubercles consisting of epithelioid cells, lymphocytes, and Langhans' giant cells that wall off the bacilli. This
corresponds to the development of delayed hypersensitivity to TB antigens that occurs around 1 to 3 weeks after inoculation.
35,96,134 By 3 weeks, a tuberculin skin test (PPD) is usually positive. 134 The tubercles that form may coalesce to form larger
nodules that are visible as oval or rounded opacities on the chest radiograph. Tubercles may continue to enlarge and undergo central
caseation necrosis, or they may heal with fibrosis and calcification. 10,96,106 Viable bacilli often survive within dormant tubercles,
only to become reactivated at a later date to cause postprimary (reactivation) TB. When liquefaction occurs in the areas of caseous
necrosis, infected material is extruded into an adjacent bronchus, leaving a tuberculous cavity behind and spreading the infection
endobronchially to other parts of the lung.
Clinically active TB develops in only about 5% to 10% of exposed people. This most often occurs as reactivation of dormant infection
sometime in the future, but it may occur as progression of primary infection or as uncontrolled dissemination if host defenses fail.
35,134 Dissemination of the tubercle bacillus is of three types: bronchogenic, hematogenous, and lymphangitic. Bronchogenic
dissemination occurs when exudate from a cavity or small area of caseation drains into a bronchus and is aspirated into previously
uninfected areas, either on the same or on the opposite side. This type of spread occurs frequently after bleeding and when there is a
cavity emptying into a bronchus. Hematogenous dissemination leads to miliary TB and to extrapulmonary lesions throughout the
body. Acute massive hematogenous spread causes miliary TB, whereas chronic spread in smaller amounts usually results in the

Primary Pulmonary Tuberculosis

Primary, or first-infection, TB occurs when the living tubercle bacilli produce a local inflammatory
process in the lung in a patient who has not been previously infected and therefore is not
sensitized to the tuberculoprotein. This form usually occurs in children. 124 The disease remains
often undetected because there are few clinical symptoms. If a roentgenogram is obtained in the
early phase, the disease resembles any other segmental pneumonic process in that it is a poorly
defined opacity, usually limited to a relatively small subsegment. In some patients, the diseased
area is larger, with one or several segments or an entire lobe involved. In susceptible persons
(e.g., blacks, poorly-nourished children), the disease may be more widespread and may
occasionally cavitate; pneumatoceles may occur. 124 The lymphangitic spread of the disease to
the hilar and paratracheal nodes results in enlargement, which may be recognizable
roentgenographically. At times adenopathy can be massive. The changes produced in the
lymphatics may occasionally be sufficient to appear as streaks of increased opacity between the
primary pneumonic disease and the hilum. If serial films are obtained, slow resolution will be noted
over 6 months to 1 year. At times the original lesion disappears so completely that it cannot be
recognized on later roentgenograms, but there is often a small nodule that later may become
calcified. The calcification within the hilar nodes and the parenchymal calcification then remain as
the only residues of primary TB. This combination of primary parenchymal opacity plus regional
node calcification is termed a primary complex or primary Ranke complex, and the parenchymal
nodule is called a Ghon tubercle. The diagnosis cannot be made on roentgen study alone, but in
many patients the appearance is so typical that the diagnosis is relatively certain. Progress
roentgenograms tend to substantiate the conclusion, and the tuberculin skin test can be used to
confirm it (Fig. 24-23). As a rule, the calcifications secondary to histoplasmosis are larger than
those in TB.

Primary tuberculosis
The
primary
pulmonary
parenchymal focus is usually
solitary but may be multiple.
There are several variations
from the typical findings
described. In some patients,
the
primary
parenchymal
opacity is so small as to be
invisible on a roentgenogram,
whereas
lymph
node
enlargement in the hilum in
the same patient may be
considerable. Distribution in
the lungs is random, so that
lower-lobe disease is at least
as common as upper-lobe
disease. The lower-lobe lesions
usually
do
not
cause
atelectasis in children, so they
often escape notice. In some
cases, no visible hilar node

A: The primary disease is noted in the left upper lung,

largely in the plane of the second anterior interspace. It
consists of poorly defined opacity in the parenchyma,
accompanied by enlarged hilar nodes. B: In a
roentgenogram obtained 1 month later, there is a clearly
defined strand of opacity extending into the area of the
previous disease. The enlarged nodes have regressed.

Tuberculous Pleural Effusion

Occasionally, the first manifestations of TB are pleural effusion and pleural
disease, which may hide the parenchymal disease. As a part of the primary
disease, pleural effusion is more common in adults than in children. The
figures vary, but about 10% of children and 30% of adults with primary TB
have pleural effusion, usually unilateral and on the side of the parenchymal
disease. In some reports, the incidence of effusion is considerably higher.
Tuberculous pleurisy develops when subpleural foci of infection rupture into
the pleural space. It can occur at any time during the course of TB, but it
most commonly occurs 3 to 7 months after the initial exposure. 35,51,96
Diagnosis is frequently very difficult, because the tubercle bacillus rarely
can be cultured from the pleural fluid.
Often a pleural biopsy is required to confirm the diagnosis. 96
Pleural effusions in primary TB usually clear completely in a month or two
without treatment. Occasionally, the effusion persists, leaving a residual sac
of fluid often encased in thickened pleura. Eventually, some of these pleural
residues may calcify peripherally or centrally and form long-term sequelae
of fibrothorax.

Atelectasis
A major cause of the opacity that is sometimes associated with primary
TB in children is now known to be atelectasis, which usually results from
compression of an upper-lobe bronchus by the large hilar nodes.
Complete occlusion may occur when there is an added factor of bronchial
infection or edema. The atelectasis may appear and disappear from time
to time, producing opacity and decreased volume of the involved lobe or
segment when present. If the atelectasis persists despite treatment with
antituberculosis drugs, it usually indicates bronchostenosis. Surgical
removal of the involved lobe may then become necessary. The more
usual course, however, is for the atelectasis to clear as the inflammatory
process subsides in the nodes and in the bronchial wall. Therefore,
roentgen findings vary in these patients. They consist of the hilar node
enlargement plus varying amounts of opacity in the involved lobe,
depending on the amount of atelectasis present in addition to the actual
tuberculous disease. The parenchymal opacity often remains after the
atelectasis clears ( Fig. 24-24). Bronchiectasis may also result as a
complication of this type of disease.

Primary tuberculosis with atelectasis. A: Note the homogeneous

opacity in the right upper lobe. The minor fissure is greatly
elevated, indicating a considerable amount of atelectasis. B: In a
roentgenogram obtained 5 weeks later, the upper lobe has
expanded. Residual pulmonary disease is present above the right
hilum; right upper hilar nodes are enlarged.

Progression
The usual course of primary TB is slow
resolution, which may occur in 3 to 9 months.
Progressive primary TB may occur in several
situations. It is most common in infants younger
than 1 year of age, in patients using
corticosteroids, and in other susceptible patients
(often with other chronic illness). The pulmonary
involvement increases; often cavitation occurs,
with subsequent bronchogenic spread or pleural
involvement with effusion and/or empyema and
occasionally with bronchopleural fistula.

Tuberculous Pericarditis
Tuberculous pericarditis usually is caused by
rupture of a caseous mediastinal node into the
pericardium. This may cause acute tamponade,
making immediate pericardiocentesis imperative.
In other cases, a more gradual accumulation of
pericardial fluid is associated with tuberculous
pericarditis. The size of the cardiac shadow
increases, and the presence of fluid can usually
be determined by echocardiography. One, now
rare, cause of calcific constrictive pericarditis is
prior tuberculous pericarditis.

Hematogenous Dissemination
and Miliary Tuberculosis
Widespread hematogenous dissemination of
TB as the result of primary infection is
uncommon but is a very serious complication
because it may lead to miliary TB and to
involvement of many extrapulmonary
structures, including the meninges. This
complication usually occurs in infants
younger than 2 years of age and is much less
common in older children. It usually develops
within 6 months of the initial primary
infection.

Other Complications
Occasionally the hilar or paratracheal
lymph nodes may become so large
that they extend into the adjacent
pulmonary parenchyma and may
require surgical removal.
Bronchoesophageal fistula has also
been reported, when caseating nodal
disease extends into the esophagus
and into a bronchus.

Primary Tuberculosis in the

Adult
Unusual pulmonary manifestations of TB have been reported because of
decreased exposure in childhood and development of the primary form of
the disease in many adults.18,102 There is more lower-lobe disease in
adults. Equal incidence or slight predominance of lower- and middle-lobe
disease has been reported. 134 Choyke and associates23 reported a 40%
incidence of lower-lobe disease and a 58% incidence of upper-lobe
disease in one series of 103 adults. Cavitation was present in 8%, which
is higher rate than that reported in children. Pleural effusion was present
in about 30%, also more common than in children. On the other hand,
adenopathy occurred in only about 10%, almost half in the right
paratracheal nodes. Others have reported a higher incidence of
adenopathy. All of the patients with adenopathy had parenchymal
disease demonstrated on chest roentgenography. In this series, about
15% of the patients were immunocompromised, so that TB can be an
opportunistic infection. ARDS occurred as a complication of miliary TB in
four patients. This is a particularly difficult situation, and prompt
antituberculosis drug therapy may be life-saving.

Postprimary (Reinfection,
Reactivation) Tuberculosis
Reinfection or reactivation TB occurs when
tubercle bacilli produce pulmonary inflammatory
disease in a person who was previously sensitized
to tuberculin. Unlike primary TB, this condition
tends to be progressive, leading to symptomatic
pulmonary disease unless treated. Lymph node
involvement is much less common than in
primary disease. The disease has a considerable
tendency to localize in the upper lobes. There is
no certain way to distinguish between the two
types on roentgen study, however.

Early Reinfection Tuberculosis

The upper lobes are the most common site, and the parenchymal disease is most often
found in the apical and posterior segments of the upper lobe. The right side is affected
somewhat more frequently than the left. However, it is not uncommon to see the initial
opacity in the superior segment of the lower lobe on either side. The basal segments of
the lower lobe are not often the site of the original disease in reactivation pulmonary TB.
The disease is asymptomatic in its early stages, and a chest roentgenogram often
indicates a lesion before the onset of subjective symptoms and before physical findings
can be elicited on examination of the chest. As far as the roentgen findings are
concerned, there is nothing characteristic about early tuberculous disease except its
location in the upper lobe, which is usually fairly peripheral in relation to the hilum.
Characteristically the disease appears as an area of mottled opacity that varies
considerably in size, and the limits of the lesion are usually poorly circumscribed. The
hazy character and poor definition of the lesions suggest a pneumonic or exudative
process, in contrast to the more clearly defined, strand-like character of chronic fibrotic
disease. It is not uncommon for this disease to be obscured to a greater or lesser extent
by the clavicle or by one of the upper ribs and thus escape attention unless the
roentgenogram is examined carefully ( Fig. 24-25, Fig. 24-26, and Fig. 24-27). In other
patients the disease may be undetected until it is well advanced, so it is not unusual to
find extensive disease with cavitation and bronchogenic spread to the opposite lung or
the lower lobe of the same lung. In others, the initial chest roentgenogram reveals a
large area of segmental or lobar consolidation representing tuberculous pneumonia.

Minimal pulmonary tuberculosis in the right upper lobe. Note the hazy, poorly defined
opacity in the first anterior interspace laterally, immediately below the clavicle. Some
disease was also concealed by the clavicle. Compare this area with the same area on the
patient's left side, which is normal. B: Somewhat more extensive disease is present in the
right upper lobe in the supraclavicular area, in the first anterior interspace, and medial to
the first rib. Some of the disease is obscured by the clavicle. The left side is normal.

Minimal tuberculosis in the left apex. The disease is clearly

defined in the supraclavicular area. It contains some calcium.
There were also several calcified nodes in the left hilum, some of
which are shown here. Note the minimal amount of pleural
thickening lateral to the pulmonary disease.

Minimal tuberculosis. A: The disease is rather poorly defined, largely in

the lateral aspect of the second anterior interspace. B: Close-up view
of the upper-right lung shows the hazy opacity to better advantage. Its
haziness and poor definition are compatible with active disease.

 At times the disease appears as a relatively clearly defined linear opacity, resembling a fibrotic scar.
However, it must be remembered that TB cannot be classified as inactive on the basis of a single
study. Because there is a wide variation in susceptibility, the virulence and number of organisms,
and the gross pathologic response to the disease, it is not surprising that roentgen study of TB
should demonstrate a wide variation in the appearance of the disease. 134 In some patients the
location and appearance of the initial tuberculous process are characteristic enough for the
radiologist to make a presumptive diagnosis of pulmonary TB, but this should always be confirmed
by bacteriologic study of sputum or of specimens obtained during fiberoptic bronchoscopy.
Recently, a number of articles have reported on the characteristic findings of pulmonary TB on CT
and high-resolution CT (HRCT) ( Fig. 24-28 and Fig. 24-29). HRCT has been shown to be more
sensitive than chest radiography for detecting early active disease. 53,56,63,67,71,72,73 and
73A,89,95,100,101 HRCT findings of postprimary TB include 2- to 4-mm centrilobular nodules or
branching structures (the tree-in-bud sign); cavities; bronchiectasis; lobular consolidation; groundglass opacities; and small (6 to 10 mm), nodular opacities. These often, although not invariably, are
seen in cases of active pulmonary TB. The tree-in-bud pattern is typical of endobronchial spread of
TB but again is not specific for TB and can be seen in other disease processes such as diffuse
panbronchiolitis, acute bronchitis/pneumonia caused by other infections, aspiration pneumonia, and
bronchiectasis of any cause with mucoid impaction. 2,7,53 The tree-in-bud sign, however, is one of
the earliest
HRCT findings of bronchogenic spread of TB. On histopathology, this sign corresponds to impaction of
caseous material within dilated, small distal bronchioles including the terminal bronchioles, the
respiratory bronchioles, and the alveolar ducts. 54

A and B: Computed tomographic findings of active tuberculosis. Multiple foci of

patchy disease are noted bilaterally, characterized by larger nodular opacities
(arrows) and surrounding areas of tree-in-bud formations ( arrowheads).

A: Chest film taken at presentation of a 34-year-old man

with a history of tuberculosis shows left pleural fibrosis
and scattered nodular opacities in both apices and in the
left lower lung. B and C: Computed tomography more
clearly demonstrates the presence of open cavities in
both apices and multiple areas of bronchogenic spread of
tuberculosis to the left and right upper lobes, lingula, and
left lower lobe. Left pleural fibrosis and bilateral calcified
hilar nodes are also present.

 CT findings associated with cases of inactive or stable TB

include fibrotic irregular lines, parenchymal bands, calcified
nodules and calcified adenopathy, architectural distortion of
the bronchovascular bundles, bronchiectasis, and pericicatricial
emphysema. 53,56,63,67,71,72 and 73,89,95,100,101 As with
chest radiographs, disease inactivity can not be determined
solely on the basis of CT findings on a single CT examination
but requires confirmation of negative sputum cultures and
serial examinations over time.
CT findings of primary TB include lobar consolidation with hilar
or mediastinal adenopathy. With intravenous contrast
enhancement, tuberculous adenopathy typically shows rim
enhancement with low-density, necrotic centers.54,72 Areas of
lung consolidation may show cavitation. 72

Bronchogenic Spread of
Tuberculosis
When enough necrosis is produced by the action of the tubercle bacillus, a cavity is formed
and the necrotic material is extruded through a bronchus. The cavity appears on the
roentgenogram as a rounded or oval area of radiolucency, usually surrounded by a
moderately thick wall and often by a considerable amount of disease in the same area.
Exudate from this cavity can be expectorated, or it may be aspirated, resulting in
bronchogenic spread of infection to other parts of the same lung or to the opposite lung.
New foci of infection are then set up that in turn may undergo eventual cavitation. Small
foci of tuberculous pneumonia are started by these bronchogenic aspirates. All of these
lesions may heal, go on to caseation and cavitation, or become productive lesions resulting
in the formation of a considerable amount of granulation tissue and eventual fibrosis. The
fibrosis may be extensive, leading to a considerable loss in lung volume and
tracheobronchial distortion.
Bronchogenic spread of TB results in a characteristic appearance on CT. In addition to the
tree-in-bud sign, CT may demonstrate patchy areas of air-space disease consisting of poorly
defined nodular opacities measuring 3 to 10 mm in diameter (see Fig. 24-28 and Fig. 2429).37,67,96 Typically, these areas of involvement are widely scattered in different parts of
the lung. An open cavity in the same or opposite lung is often identified. The nodular
opacities of bronchogenic spread are less uniform, less well marginated, larger, and less
evenly distributed than the smaller (1 to 3 mm), discrete nodules of miliary TB. 67,96 Not
surprisingly, CT often reveals more extensive bronchogenic spread of TB than is
appreciated on the chest radiograph (see Fig. 24-29).67,96

Cavitation
The presence of cavitation in a patient with pulmonary TB is common and is often readily detected
roentgenographically because the cavity is large enough to produce a distinct round or oval radiolucency with a
moderately thick wall. If there is uncertainty about the presence of a cavity, CT should be used to confirm or exclude
its presence (see Fig. 24-29). CT is very valuable in detection of cavitary disease and is more reliable than chest
radiography.
As with other aspects of tuberculous disease, there is wide variation in the appearance of tuberculous excavation
from one patient to the next. The cavitations appear as radiolucent areas that vary widely in size but are generally
round or oval. The inner wall of a cavity may be smooth or irregular ( Fig. 24-30). The walls are usually moderately
thick except in tension cavities, which become fairly large and may exhibit thin walls. A tension cavity develops
because a check-valve type of obstruction of the bronchus leading to it allows air to enter the cavity more freely than
it can escape. This type of cavity may disappear very quickly after treatment is instituted, because the bronchial
obstruction that contributed to its size may be relieved quickly and permit the cavity to collapse. Thick-walled
cavities, on the other hand, often show little tendency to close, or they may close or decrease in size very slowly
when treated. Although not as common as in lung abscess, fluid can occasionally be present in a tuberculous cavity,
so fluid levels can be demonstrated on horizontal-beam roentgenograms or CT. Airfluid levels, however, may also be
an indication of superimposed bacterial or fungal infection in a chronic tuberculous cavity. 35,67,96 In general, the
walls of the cavities decrease in thickness and become less distinct as the disease regresses under treatment.
Fibrosis, with contraction of the previously involved lung, and emphysema may result in production of irregular or
oval radiolucencies that simulate cavities very closely. In these instances it is often difficult and sometimes
impossible to differentiate a thin-walled cavity from an area of emphysema unless the disease has been well
documented by repeated roentgenograms during its course. In these patients, CT is often of considerable value.
If cavitation or extensive disease has occurred in a lobe or segment, fibrosis is a part of the healing process and
results in volume loss, often with bronchial, hilar, and mediastinal distortion.
Tuberculous disease activity can not be determined on the basis of radiographic or CT appearance of the cavity
alone, and diagnosis must be made from results of sputum cultures and serial imaging analysis. 35,67,96 Even
chronic cavities can continue to discharge viable bacilli.

Advanced bilateral pulmonary tuberculosis. A: Note the large apical cavity on the
right in the supraclavicular area. The disease is extensive in the upper half of both
lungs, and several suspicious radiolucent areas are noted on the left. B and C: In
tomograms of the patient shown in A, the apical cavity on the right, some shift of
the trachea to the right, and several small cavities on the left are evident.

Bronchiectasis
Endobronchial involvement in pulmonary TB is very common and leads to
bronchiectasis in many instances. The presence of bronchiectasis in patients with TB
can often be diagnosed or at least suspected on routine roentgenograms, because
the thick-walled bronchi filled with air stand out in contrast to the diseased lung
surrounding them. In other cases, particularly in less extensive disease, the diagnosis
can be made with a high degree of certainty on CT. If the extent of bronchiectasis is
to be determined before surgical removal, bronchography or, more commonly, CT is
used to make this assessment. Bronchiectasis in patients with pulmonary TB may be
saccular or cylindrical and is found in the lobe or segment involved by the disease.
Occasionally, it is detected in an area where there is no obvious parenchymal
involvement. Presumably, the bronchiectasis was caused by tuberculous disease
which has resolved to the point where no roentgen evidence of parenchymal
involvement remains. For this reason, many investigators consider that CT or
bronchography is indicated before segmental surgery is undertaken in patients with
pulmonary TB. Because antituberculosis drug therapy is very effective, surgery is
now limited to the occasional patient with severe bronchiectasis, hemorrhage, or
repeated infection localized to the site of earlier TB. There is some difference in the
appearance of bronchiectasis in TB compared with that caused by other conditions. In
TB there is often peripheral obliteration and more fibrosis with greater distortion of
bronchi ( Fig. 24-31).

 Bronchiectasis in tuberculosis (TB). A: Note the

dilation of the upper-lobe bronchi, which are
also crowded in a patient who had previous
extensive TB of the right upper lobe. There is
very little alveolar filling, and the distal ends of
the bronchi are obstructed. The latter finding is
characteristic of TB. B: Bronchogram of a
patient with far-advanced TB of long duration.
The right upper lobe is contracted, and there is
extensive saccular bronchiectasis, bronchial
distortion, and failure of parenchymal filling.

Bronchiectasis in tuberculosis
(TB). A: Note the dilation of
the
upper-lobe
bronchi,
which are also crowded in a
patient who had previous
extensive TB of the right
upper lobe. There is very
little alveolar filling, and the
distal ends of the bronchi are
obstructed. The latter finding
is characteristic of TB. B:
Bronchogram of a patient
with far-advanced TB of long
duration. The right upper
lobe is contracted, and there
is
extensive
saccular
bronchiectasis,
bronchial
distortion, and failure of
parenchymal filling.

Unusual Radiographic Manifestations

of Pulmonary Tuberculosis
In addition to the unusual distribution and other differences described in adults with
primary TB, several other possible findings should be mentioned:
1. Multiple bilateral large pulmonary nodules.
2. Multiple small, scattered, cavitary foci that resemble hematogenous staphylococcal
abscesses. These lesions remain unchanged and can therefore be differentiated from
acute staphylococcal disease, which changes rather rapidly.
3. Pulmonary gangrene resulting from TB. The patients are very ill and this disease is often
fatal. A large, homogeneous, lobar alveolar process is observed to increase in density; the
lobe increases in volume, and cavitation appears with a large intracavity mass of necrotic
tissue, similar to that sometimes observed in Klebsiella pneumonia.62
4. Rasmussen aneurysm, a rare pseudoaneurysm caused by erosion of a peripheral
pulmonary artery branch within a tuberculous cavity. It can simulate a mass within a
cavity. Complications include formation of an arteriovenous fistula, rupture with
hemoptysis, and sometimes exsanguination. These aneurysms can be treated by
embolization to occlude the involved pulmonary artery branch.
5. A nonspecific severe, widespread interstitial pattern throughout both lungs. This occurs
in middle-aged and elderly patients with emphysema. The patients are not very ill, and
there is no radiologic change over many months. Diagnosis is usually made by open lung
biopsy. Response to good antituberculosis drug therapy is very slow. Pneumothorax may
complicate this unusual form of TB. 102

Tuberculosis in the
Immunosuppressed Patient
The cell-mediated immune response (T lymphocytes) is largely involved in the
destruction of tubercle bacilli. There are several situations in which cellmediated immunity is depressed.93 They include acquired immunodeficiency
syndrome (AIDS) (see Chapter 25),104A aging, starvation, chronic illness,
alcoholism, cancer, sarcoidosis, silicosis, pregnancy, radiation, and drugs such
as corticosteroids, immunosuppressive drugs, and cytotoxic drugs used in
cancer chemotherapy. Patients with these conditions are at risk if exposed to
the organism. The highest incidence appears to be in elderly persons,
debilitated persons, and patients with AIDS, chronic diseases, or malignancy.
Although TB is difficult to manage in patients with silicosis, the incidence of
TB in patients with silicosis is decreasing. Whether this will remain true in the
future is not certain, since the incidence of TB may be increasing.
The radiographic appearance of TB depends on the level of
immunosuppression. It is similar to that in other patients except when T-cell
depression becomes significant. Then the disease is likely to progress more
rapidly, to become far advanced, and to develop miliary spread. This can
occur in primary as well as in reactivation TB.

Tuberculoma
The term tuberculoma refers to the round, focal, tuberculous lesion that may be solitary or multiple. There are
many inflammatory nodules in which tubercle bacilli cannot be found. The histopathologic findings are
nonspecific. They are termed chronic nonspecific granuloma and cannot be differentiated from tuberculoma by
roentgenographic methods. The tuberculous nodules vary in size from a few millimeters to 5 or 6 cm but usually
range from 1 to 3 cm. They may or may not contain calcium and usually contain caseous debris. Small flecks of
calcium may be scattered in the lesion, and in some instances calcium may form a more or less complete shell or
ring in or near the outer wall of the nodule. Several concentric rings of calcium or an eccentric or central nidus of
calcium may be present. The pathogenesis is varied, and the nodule may represent either primary or reinfection
disease. Sometimes the nodule results when a cavity is sealed by obstruction of its draining bronchus. It may
also be a residual localized area of caseation that persists when the remainder of the primary disease clears. It is
not unusual to see a few tiny satellite nodules or poorly defined areas of opacity in the vicinity of a tuberculoma.
All of these lesions are potentially dangerous, because they may contain viable tubercle bacilli for long periods
and may break down at any time with resultant dissemination of the disease. They may remain constant in size
or grow very slowly over a period of years.
The roentgen finding is that of a round parenchymal nodule. If concentric rings of calcium are visible, the lesion
is almost certainly a tuberculoma or other chronic inflammatory granuloma (Fig. 24-32). If no calcium is
demonstrated on the routine roentgen study of the chest, CT is indicated. Calcium can often be seen on CT when
its presence is not detected on the preliminary film. If no calcification is found, differentiation of the tuberculoma
or other infectious granuloma from bronchogenic carcinoma, other lung tumors, or solitary pulmonary metastasis
may be impossible. Recent preliminary studies by Swenson and others suggest that small noncalcified nodules
that fail to show significant contrast enhancement on dynamic serial CT scanning while intravenous contrast is
being administered are likely to be benign. 129A In the patient with a small, solitary nodule that is not clearly
benign, resection must be considered, unless previous films from 2 or 3 years ago indicate that the lesion has
been present for a long time and is unchanged. Transbronchial or percutaneous needle biopsy may clearly
demonstrate granulomatous disease. If there is doubt or if malignancy is found, resection is necessary.

Tuberculoma
Note
the
dense,
calcified nodule in the
right midlung. Some
disease is also noted
lateral to it and above
it in the lateral aspect
of the second anterior
interspace.
Some
calcified hilar nodes are
noted bilaterally.

Healing of Pulmonary
Tuberculosis
In general, pulmonary TB heals slowly, so that it is possible by serial roentgenography to follow
the gross anatomic changes in the disease. Differences can be noted in the manner of healing,
which depends on the type of involvement and the susceptibility of the tubercle bacilli to the
antituberculosis drugs as well as on the response of the patient. Complete resolution often
occurs in some areas. It is a common observation that complete resolution occurs and is most
striking in patients with relatively acute disease in which the process is presumed to be largely
exudative ( Fig. 24-33). This accounts for the decreased thickness of the walls of cavities that is
often noted in patients undergoing treatment. The exudative portion of the process making up
the cavitary wall resolves, resulting in a decrease in thickness. In patients in whom the disease
has progressed to the point of necrosis, complete resolution is not possible. In these patients,
fibrosis with contraction of the scars results in shrinkage in the volume of the involved lobe or
segment and sometimes a decrease in the size of the hemithorax. The mediastinal structures
are retracted to the side of involvement. The hilum is elevated in upper-lobe disease, and
sometimes the hemidiaphragm is raised. The lesions that contain granulation tissue as well as
caseation, and are often noted as poorly defined nodules, show gradual reduction in size. The
individual nodules tend to become more clearly defined on the roentgenogram, evidently also
because of contraction and fibrosis. This type of lesion often is the site of calcium deposition
and in some instances becomes densely calcified with the passage of time. Many of the lesions
contain central areas of necrosis in which viable organisms can be found after long periods of
apparent inactivity. In summary, as visualized roentgenographically, there is considerable
difference in the healing process from one patient to another, but it is unusual to see the
disease disappear entirely ( Fig. 24-34).

Far-advanced bilateral pulmonary tuberculosis, showing the regression resulting from

treatment with antituberculosis drugs. A: Note the extensive bilateral disease.
B: Study made 9 months later shows great improvement. The remaining disease
consists largely of fibrous strands with a few nodules in each lung.

Far-advanced pulmonary tuberculosis. A: Initial film

shows the bilateral disease. A large cavity in the right
apex is rather poorly defined on this film. B: Nine
months later, the right lung shows the result of
treatment. The large apical cavity is more clearly
defined. The upper lobe is contracted, but much of
the exudative disease has cleared. C: Sixteen months
after the initial examination, most of the residual
disease has been resected and now the findings are
those of surgical scarring in the right second anterior
interspace and in the left subclavicular area.

 CT is very helpful in demonstrating nodular residuals that cannot

be clearly defined on routine chest roentgenography. Examination
of surgical specimens has demonstrated that it is very difficult to
be certain on roentgen examination that no residual disease is
present.
Roentgenographic changes observed during the healing process
have very little prognostic value. Studies have shown that it is not
necessary to take routine follow-up roentgenograms when a
patient undergoing treatment has no clinical signs to warrant
concern. After treatment, chest radiographic study is necessary if
symptoms recur. When examining a patient with residuals of TB,
it is imperative to compare the earliest available chest film with
the current one, because changes are subtle and gradual and
may be overlooked if only the most recent film is used for
comparison.

Complications of Reinfection Pulmonary

Tuberculosis: Pleural Effusion and Empyema
Because pulmonary TB is a peripheral lesion, pleural involvement is common ( Fig. 24-35); effusion
may be found in patients without an obvious pulmonary lesion. In some instances the opacity
produced by the fluid obscures the parenchymal disease. In others, pleural effusion is the only
roentgen manifestation and, even when the fluid has been removed or absorbed, no definite
pulmonary parenchymal focus is roentgenographically visible. In some patients the fluid disappears
spontaneously or can be successfully aspirated, and in others tuberculous empyema results.
Occasionally, the pleural space may be involved by secondary infection. The tuberculous empyema
is similar to empyema of nonspecific origin in its roentgen appearance. It is usually loculated and
may become very large. If it is present and undrained for a long time, calcification may occur,
producing marked radiographic opacity outlining the wall. Bronchopleural fistula may also occur, with
drainage of all or part of the contents of the empyema and entrance of air into it. Pleurocutaneous
fistula and bronchopleurocutaneous fistula are rare complications of chronic TB. In some patients
with tuberculous pleural disease, considerable fibrosis in the pleural space results in marked pleural
thickening and constriction of the adjacent lung or of the entire hemithorax if the disease is
extensive, so-called fibrothorax. Calcification may then occur in or adjacent to either the visceral or
parietal pleura or both.
Occasionally, an empyema develops years after the initial pleural infection and should be suspected
if the volume of the fibrothorax increases. The presence of fluid within the pleural space or between
the layers of fibrothorax can be detected by ultrasonography in most instances; CT may also be
useful in this situation, particularly if ultrasonography is equivocal. If the pleural infection remains
active, chest wall extension of the empyema may develop; this is called empyema necessitatis.

Pulmonary tuberculosis, showing the development of pleural effusion.

A: Bilateral tuberculosis of the upper lobe is manifested by opacity
that is rather homogeneous and more intense on the right than on the
left. There is no evidence of pleural fluid on the right, and there was
none on the left. B: Four weeks later, a large pleural effusion on the
right is evident. Note that the parenchymal disease has regressed
slightly owing to treatment during the interval.

Bronchostenosis
Narrowing of a bronchus may result from pressure of
an enlarged lymph node that is involved by TB. This is
usually found in children with primary TB. It is also
caused by endobronchial inflammation and granuloma
formation or fibrosis in the postprimary or reinfection
form of the disease. Roentgen findings are not evident
until the obstruction is sufficient to cause either
atelectasis or obstructive overinflation. Broncho
stenosis may also result in repeated nonspecific
infections distal to the narrow bronchus. Complete
bronchial occlusion as the result of tuberculous fibrosis
rarely may be the cause of mucoid impaction.

Broncholithiasis
Occasionally, a calcified node adjacent to a bronchus
erodes into the bronchus and the calcified material from
the node is extruded into the bronchus, producing a
broncholith. This may cause very few symptoms or on
rare occasions it may result in bronchogenic spread of
tuberculous disease or hemorrhage. The calcification
may also cause bronchial obstruction with overinflation
or atelectasis. This complication may also occur in
patients with calcified nodes caused by lesions other
than pulmonary TB. Radiographic findings vary with the
situation. The calcified nodes are often visible, and their
relationship to the bronchus can best be determined by
CT (Fig. 24-36).

Computed tomogram demonstrates a broncholith protruding

into airway of the bronchus intermedius near the take-off of
the middle-lobe and lower-lobe bronchi.

Tuberculous Pneumothorax
When pneumothorax complicates pulmonary TB, it creates
the hazard of widespread pleural involvement leading to
tuberculous empyema and bronchopleural fistula.
This is because the pneumothorax often results from
rupture of a caseous subpleural focus into the pleural
space in advanced disease. It is also possible for a small
subpleural bleb to rupture, leading to a simple
pneumothorax that resolves quickly without further
complication. The roentgen appearance is similar to that
noted in pneumothorax from other causes, but the
tuberculous disease is visible and a considerable amount
of adhesive pleuritis may result in irregular or loculated
pneumothorax. This is an uncommon complication of TB.

Dissemination to Other Organs

Patients with pulmonary TB occasionally develop
disease in other organs and systems such as the
larynx, ileum and cecum, urogenital organs, and
skeletal system.
Gastrointestinal disease and laryngeal disease
are frequently the result of contact with sputum
and only rarely indicate a hematogenous spread.
On the other hand, renal TB or skeletal
involvement indicates hematogenous or
lymphangitic spread. These lesions are discussed
by organ or system in the appropriate chapters.

Hematogenous Tuberculosis
Hematogenous pulmonary TB includes several types of disease.
When the organisms enter the blood stream, it is possible to get
hematogenous involvement of numerous other organs and systems.
The actual mode of dissemination is difficult to determine in any
specific instance, but dissemination may occur by way of the
lymphatics and enter the bloodstream through the thoracic duct, by
direct rupture of a caseous focus into a vessel, or by formation of a
subintimal tubercle that serves as a source of organisms. The
invasion of the bloodstream may occur in any stage of TB. When
hematogenous dissemination develops, numerous factors have a
bearing on the resultant disease, including the age of the patient, the
number and virulence of the organisms entering the bloodstream,
the individual and racial susceptibility, the general health of the
patient, and the patient's state of allergy and immunity at the time of
the invasion. Prompt treatment with antibacterial drugs usually alters
the disease considerably in a favorable manner.

Miliary Pulmonary Tuberculosis

Two clinical types of miliary TB are recognizedacute miliary TB and subacute or chronic miliary
pulmonary dissemination. Miliary dissemination can occur at any time after the primary
infection.35 Acute miliary TB follows massive bloodstream invasion and produces a severe
acute illness, frequently with fatal termination before the use of antituberculosis drugs. In
infants and children it may result by spread from a primary site and produces severe clinical
manifestations. It usually occurs in malnourished or chronically ill infants, who are unusually
susceptible. In most children, however, the number of organisms is small and host resistance
sufficient to prevent miliary spread of the disease, so there are no clinical manifestations. In
adults, particularly in the older age group, the disease may be insidious and extremely difficult
to recognize. Findings on chest roentgenograms depend on the size and number of miliary
tubercles. The actual nodules visualized on a roentgenogram are the result of superimposition
of many small parenchymal lesions that create sufficient opacity to be recognized as a small
nodule. In the typical patient the appearance is that of a fine granularity or tiny nodulation
scattered uniformly throughout both lungs. At times the lesions are rather clearly defined as
innumerable fine nodules, each sharply delineated; in other patients they are less sharply
outlined, with hazy margins ( Fig. 24-37 and Fig. 24-38). In some patients with miliary
pulmonary TB, no lesions can be seen on the initial chest film, but in most instances a classic
miliary pattern develops during the course of the disease. 39
Because miliary disease in adults can take up to 6 weeks to become apparent on chest
radiographs, 6,43,47,96 CT may be helpful in detecting the disease earlier. In cases of miliary
TB, CT demonstrates innumerable 1- to 3-mm, discrete nodules randomly distributed
throughout the lungs 72 (Fig. 24-39).

Miliary
tuberculosis.
Close-up view of
the right upper
lung in a patient
with miliary
tuberculosis
shows the
numerous small
opacities along
with a small
increase in
interstitial
markings.

Posteroanterior
(A)
and lateral (B) views
showing
miliary
tuberculosis.
Note
the extensive miliary
nodules, more dense
and clearly defined
than those in FIG. 2437. The patient had
weight loss, fever,
and a cough.

A and B: Miliary tuberculosis. Computed tomography demonstrates widely

disseminated tiny nodules of uniform size and uniform distribution.

 Some findings may suggest TB on the initial chest radiograph, however. Pleural involvement is common,
resulting in unilateral or bilateral pleural effusion that varies considerably in amount. Rarely, recurrent
pneumothorax complicates the disease. The cause is not certain, but subpleural caseating nodules may
rupture into the pleural space in some instances. The individual lesions are largely exudative, and when
treatment with antibacterial drugs is effective, the widely scattered foci usually disappear completely. They
do not result in scattered pulmonary calcifications.
The differential diagnosis of miliary TB is often difficult from a roentgen standpoint because numerous
other diseases produce widespread scattered and miliary type of nodulation in both lungs. Correlation of
clinical and roentgen findings is very important in all instances. Several acute processes cannot be
differentiated from miliary TB on a single chest roentgenogram. Miliary bronchopneumonia, which may be
of viral or bacterial origin, and bronchiolitis in children that results in widespread miliary nodulation may
closely resemble miliary TB. In other diseases such as sarcoidosis, the pneumoconioses, and miliary
pulmonary carcinomatosis, the history and clinical course usually permit differentiation. Several additional
conditions can produce acute, diffuse miliary lesions in the lung. They include other bacterial infections
such as staphylococcal and streptococcal pneumonia, viral and rickettsial infections such as chickenpox
and Q fever, mycotic infections such as histoplasmosis and blastomycosis, and parasitic infestations such
as schistosomiasis. Also included are the noninfectious diseases, acute berylliosis, miliary hemorrhages,
and acute, diffuse, interstitial fibrosis as described by Hamman and Rich. It is therefore evident that the
roentgen findings must be correlated with the results of clinical and laboratory examinations. In some
instances, serial roentgenograms, spaced over a period of days or weeks, are helpful in establishing the
diagnosis.
In the immunocompromised patient and the infant with acute febrile illness and miliary pulmonary
disease, and in difficult cases in elderly patients, lung biopsy to get a prompt diagnosis may be indicated,
since a delay in treatment could be fatal.

Subacute and Chronic Hematogenous

Pulmonary Dissemination
Subacute and chronic hematogenous pulmonary dissemination is a
somewhat different clinical entity from acute miliary TB in that it is often
asymptomatic. Repeated small episodes may occur, so that lesions,
although widespread and distributed rather uniformly throughout both
lungs, are likely to be somewhat more variable in size than in the acute
miliary process. When this type of dissemination is extensive, the
roentgen findings are similar to those in the acute type of miliary TB, but
there is considerable difference in the clinical course. In other instances
the hematogenous pulmonary dissemination may be relatively localized,
producing small, poorly defined, rounded or oval areas of density in a
segment or lobe. Some of these nodules may regress, and others may
coalesce to form larger nodules; these may heal in a manner similar to
that described for reinfection TB. In patients with far-advanced
pulmonary TB and a considerable amount of cavitation, there may be
hematogenous spread to the lower lobes or to the opposite lung,
resulting in scattered lesions that cannot be differentiated from the
secondary lesions produced by bronchogenic spread of the disease.

Atypical Mycobacteria
Some Mycobacteria species that can cause pulmonary disease that is
similar to TB caused by M. tuberculosis but slightly different from the
standpoint of roentgen findings. These mycobacteria have been classified
according to growth characteristics when exposed to light into four
groups 133:
Group I. Photochromogens: M. kansasii, M. marinum, and M. simiae
Group II. Scotochromogens: M. scrofulaceum, M. szulgai, and M. gordonae
Group III. Nonphotochromogens: M. avium-intracellulare (Fig. 24-40), M.
nonchromogenicum, M. terrae, M. novum, M. triviale, M. xenopi, M.
malmoense, and M. ulcerans
Group IV. The rapid growers: M. fortuitum, and M. chelonei
The clinical and radiologic aspects have been discussed at length by
Wolinsky, 132 Woodring and Vandiviere, 133 and others.3,25,107,121 The
most important of these pulmonary pathogens are M. aviumintracellulare, M. xenopi (particularly in Ontario121) (Fig. 24-41), and M.
kansasii.

A and B: Atypical mycobacterial infection caused by Mycobacterium aviumintracellulare in a middle-aged white woman with chronic cough. Computed
tomogram shows focal bronchiectasis and some surrounding inflammatory
disease in the left lung apex and a cluster of nodular opacities and tree-in-bud
pattern in the lateral aspect of the right upper lobe. Calcified granulomas are
noted in the right hilum. Group

Atypical mycobacterial infection caused by

Mycobacterium xenopi. A: A large cavity with an
airfluid level is present in the right upper lobe,
and a calcified granuloma is noted in the left
lower lung. B and C: Computed tomogram
demonstrates a thick, irregular, walled cavity
with airfluiddebris level. Bronchiectasis in
noted medial to the cavity, and one of the
dilated bronchi communicates with the cavity
( C).

M. avium-intracellulare (M. avium complex) infections appear to be increasing, particularly in persons with decreased
cellular immunity or chronic lung disease, but also in those without predisposing cause. The radiologic features are
slightly different from those of M. tuberculosis and show the following contrasts:
1. There is an increase in cavitation in relation to the amount of lung involved.
2. Thin-walled cavities without much surrounding disease are seen; cavities may be small. However, in general,
cavities caused by atypical mycobacteria are
indistinguishable from those caused by M. tuberculosis.3,25,84
3. Spread is more often contiguous than bronchogenic.
4. The anterior segment of the upper lobe appears to be involved more frequently than in M. tuberculosis.
5. There is marked pleural thickening over the involved areas of lung.
6. There is more involvement of apical and anterior segments of the upper lobes.
7. Clustered opacities around irregular translucent areas with radiating line shadows are seen; opacities resembling
tumors occasionally occur.
8. Disease is usually unilateral even when far advanced.
9. It is usually found in older age groups.
10. Pleural effusion is uncommon and small in amount.
11. Adenopathy is uncommon.
12. Disease is often extensive when first discovered.
13. There is a marked predominance of whites to blacks (10:1).
Although these findings differ somewhat from those in TB, the variety of findings in M. tuberculosis infections is such
that roentgenographic differentiation cannot be made. At times atypical mycobacterial infection can be suggested,
however. These atypical organisms usually do not respond well to antituberculosis drug therapy. M. avium complex
appears to be particularly difficult to control; surgical removal of residual disease may be necessary and should
perhaps be considered after antituberculosis therapy.

Surgical Measures in Pulmonary

Tuberculosis
Despite the undoubted value of the various antibacterial drugs now available for
the treatment of TB, in some patients cavities fail to close or tubercle bacilli
continue
to be discharged in pulmonary secretions. Tuberculous bronchiectasis may cause
repeated hemorrhage, may cause repeated nonspecific infections, or may harbor
an
aspergilloma, which can also cause bleeding and be difficult to eradicate. These
patients then become possible candidates for surgery, which is usually a
resection of
the residual disease. The roentgen findings after pulmonary resection for TB are
similar to those described in Chapter 31.
Before effective drugs were available, thoracoplasty and plombage were used in
an attempt to close cavities and promote healing. Thoracoplasty is used very
rarely
today, and plombage is no longer used. Older patients who have had these
procedures may be examined by means of chest films, so examples of patients
who have
undergone these procedures are included ( Fig. 24-42 and Fig. 24-43).

Left thoracoplasty. This

surgical procedure, which
was used extensively
before the advent of
antituberculosis drugs, is
employed rarely at present.
There has been extensive
resection of the upper
seven ribs on the left,
compressing the left upper
lung. Regeneration of the
ribs has formed a solid
bony plate along the upper
lateral chest wall. The
scoliosis is a common result
of thoracoplasty.

Lucite-ball
plombage.
Although this procedure has
been
abandoned,
occasionally
patients
are
observed with the rounded
lucencies representing Lucite
balls, usually at the apex of
one hemithorax, as in this
patient.

Complicating Aspergillomas
Chronic tuberculous cavities may
remain open long after sterilization
and become colonized by Aspergillus
organisms that develop into fungus
balls or aspergillomas11

ACTINOMYCOSIS
Actinomycosis in humans is caused most commonly by an anaerobic organism, Actinomyces israelii. This organism
occurs as a filamentous, gram-positive, nonacid-fast, rod-shaped bacterial form in the mouth and as a mycelial form in
infected tissues. 69 Other actinomycetes can cause human infection, including A. bovis, A. naeslundii, A. ericksonii, A.
meyeri, and A. propionicus. The organisms are now established as bacteria, but roentgen and clinical findings are often
similar to those of mycotic infections in that they produce chronic suppurative infections. 69,122 The disease may
affect any part of the body but is found most frequently in and about the jaw (the cervicofacial form of the infection).
There is also an abdominopelvic form, often associated with appendiceal surgery or use of intrauterine devices, and a
thoracic form of the infection.4,69 Pulmonary infection is said to occur in approximately 15% of patients with the
disease. However, in recent years, the incidence of pulmonary involvement has declined considerably; the classic
empyema with chest wall sinus tracts and pulmonary parenchymal disease is rarely seen and is avoided by timely
antibiotic therapy. Occasionally, however, it is still encountered as a complication of thoracic surgery or in debilitated
patients such as alcoholics or those with COPD.69 This form of the disease is characterized by its tendency to produce
suppurative sinus tracts and its ability to cross tissue planes that provide a barrier to the usual infections. Drainage
from actinomycosis sinus tracts demonstrates sulfur granules, a hallmark of the infection. 4,69
The roentgen findings vary greatly. The disease may be unilateral or bilateral but tends to be unilateral unless widely
disseminated. It produces a dense, confluent opacity in the affected lung, usually in a lower lobe peripherally, in which
cavitation may be present ( Fig. 24-44 and Fig. 24-45). The cavity may persist after treatment as a thin-walled, cystic
shadow. In the classic chest wall disease, pleural involvement results in varying amounts of pleural thickening and fluid.
Infection of the chest wall causes soft-tissue swelling and may cause periosteal reaction and/or destruction of ribs with
sinus tract formation. This is characteristic of advanced disease, which is now observed infrequently. The parenchymal
involvement may resemble acute alveolar pneumonia in some instances. In other cases, the disease is manifested as a
local, mass-like opacity resembling bronchogenic carcinoma. Another roentgen pattern is that of a fan-shaped
consolidation near the hilum or radiating from the hilum into the superior segment of the lower lobe. Rarely,
hematogenous spread from a focal area of disease results in a miliary pulmonary pattern.
When the combination of pulmonary disease and chest wall involvement with empyema and sinus tracts is present,
actinomycosis may be strongly suspected. However, it must be differentiated by bacteriologic examination from TB,
chronic fungal infections, Nocardia, and tumors.

Actinomycosis
The dense, confluent
consolidation in the
left
lower
lung
obscures
the
left
hemidiaphragm
and
left
lower
cardiac
border. The patient
also had a chest wall
mass and sinus tracts
typical of this disease.

A and B: Actinomycosis infection of the chest wall. Computed tomogram

shows a chronic draining sinus tract that can be traced from the skin surface
into the abdomen, through the diaphragm, and into the right pleural space.

 CT findings of thoracic actinomycosis include air-space

consolidation with adjacent pleural thickening. Hilar or mediastinal
lymph nodes (usually measuring less than 2 to 2.5 cm) are seen in
75% of patients on CT. Like adenopathy, cavitation and
microabscesses are appreciated more often on CT than on
conventional plain films in this infection.4,69 With chest wall
invasion, inflammatory chest wall masses, abscesses, and sinus
tracts may be identified on CT. 4 MRI is probably superior to CT in
demonstrating the extent of soft-tissue infection and sinus tract
formation, since both of these demonstrate high signal intensity on
T2-weighted images. CT, however, is better for demonstrating rib
and bone destruction and periostitis. Traditional sinograms with
contrast injection of sinus tracts may also be needed to follow the
course of these sinuses. Infections and sinus tracts have been
known to communicate to the pleural space, to the chest wall, to
the mediastinum, and through the diaphragm (Fig. 24-45).69

NOCARDIOSIS
Nocardia asteroides is the most common of several species of Nocardia that
can cause disease. It is an aerobic, gram-positive, filamentous, beaded acidfast bacterium. It is recognized increasingly as an opportunistic infection in
patients with underlying chronic debilitating disease or immunodeficiency,
particularly in those who have undergone therapy with immunosuppressive
or cytotoxic agents or steroids, including patients with cancer, organ
transplants, diabetes mellitus, or chronic liver disease. Patients with
congenital immune deficiencies and those with AIDS are also at risk. 16,112
In nocardiosis, pulmonary roentgen findings are varied. They may be similar
to those of actinomycosis, mycosis, or TB and consist of homogeneous
segmental or lobar air-space consolidation; or they may consist of one or
more discrete nodules or rounded opacities. Cavitation is common. 16,44
Pleural involvement with empyema and chest wall invasion can also occur
with Nocardia, and extrapulmonary dissemination to the central nervous
system, cutaneous sites, and elsewhere have been reported ( Fig. 24-46,
Fig. 24-47 and Fig. 24-48).16 The disease is frequently bilateral. It crosses
fissures and anatomic barriers if not properly treated, but not as frequently
as actinomycosis.

 On CT, the most common finding is one or more nodules or mass-like opacities which may or may not
undergo cavitation. When compared with conventional radiography, CT shows more nodules and is
better for characterizing the extent of disease (see Fig. 24-48).16 CT is also useful for localizing
lesions when aspiration or biopsy is needed for diagnosis. This is often required, because isolation of
Nocardia from sputum is difficult owing to the organism's slow growth and prolonged incubation
period of up to 5 weeks. 16 The diagnosis is often elusive until material for histologic study is
obtained by aspiration lung biopsy, transbronchial aspiration, bronchial brushing, or open lung
biopsy.
Pulmonary nocardiosis can present as an acute pneumonia, as a subacute process, or as a chronic
indolent infection with prominent constitutional symptoms of fever, weight loss, and malaise.16 The
roentgen alterations in the lungs persist for long periods, frequently with little change unless the
patient is treated with appropriate antibiotics. It is not unusual for the disease to run a protracted
course with very little variation in the appearance of the pulmonary lesions and very few symptoms.
Pleural involvement with empyema and extension to involve the ribs with production of chest wall
abscess is not as common as in actinomycosis but can be seen with nocardiosis. Occasionally,
Nocardia may involve the skin when inoculated in a traumatic event. Then, extremely rarely, it may
spread through the bloodstream to the lungs to produce disseminated pulmonary disease.
Mediastinitis with adenopathy and obstruction of the superior vena cava has been reported.
Nocardiosis is one of the few benign diseases that can cause obstruction of the superior vena cava.
104 In addition to differentiation of this disease from TB, the other chronic infectious lesions of the
lungs must be included in the differential diagnosis. Identification of the causative agent is necessary
to confirm the diagnosis.

Nocardiosis. A: This film shows a small amount of poorly defined opacity at the
right base just above the diaphragm. B: Roentgenogram obtained 9 months later
shows extensive progression of the disease with large, poorly defined nodular
and patchy opacity in both lungs. A large homogeneous consolidation in which
there is a cavity (arrow) is seen in the right upper lobe. There has been open
drainage of the pleural space in the right upper anterolateral chest wall.

Necrotizing cavitary pneumonia

caused by Nocardia infection

MYCOTIC DISEASES OF THE LUNG

Mycotic diseases of the lung are caused by a variety of organisms, many of
which are capable of producing acute lung disease (e.g., pneumonia, lung
nodules), chronic stable or slowly progressive lung disease, or disseminated
multiorgan infection. 86 Some fungal species are saprophytes or are of very
low virulence, but in compromised hosts they may produce life-threatening
acute pneumonia. The diseases must be differentiated from each other,
from pulmonary TB, and occasionally from lung tumor. The ultimate
diagnosis depends on demonstration of the causative agent in bronchial
secretions or in sections of the lung. In some instances studies based on
immunologic reactions are sufficient. These consist of skin tests,
agglutination, complement fixation, and precipitation reactions. 119
The gross anatomic changes in pulmonary disease produced by these varied
organisms may be similar. On the basis of roentgen examination it is often
possible to indicate only that the lesion is a chronic inflammatory disease of
unknown origin. At other times it is possible to make the diagnosis with a
considerable degree of accuracy on the basis of clinical findings correlated
with roentgen manifestations.

Coccidioidomycosis
Coccidioidomycosis is caused by the fungus Coccidioides immitis.28 It is an endemic pulmonary disease occurring in the arid southwestern part of the United States,
particularly in the San Joaquin valley in California and in southern Arizona. Primary pulmonary coccidioidomycosis is usually asymptomatic and is discovered
incidentally on a chest film (60%). There may be calcified granulomas in the lung or hilar nodes; in other cases, there may be a focus of pulmonary fibrosis or pleural
thickening, and in some there may be no recognizable residual. If a chest film is obtained during the asymptomatic acute phase, a focus of alveolar pneumonia may be
observed. The primary or initial infection may also produce an acute pneumonia associated with symptoms of an acute pulmonary disease, including fever, malaise,
headache, and cough. Erythema nodosum is a common clinical manifestation during the acute febrile illness, and in the San Joaquin valley this clinical syndrome is
known as valley fever. Erythema nodosum is often associated with arthralgias and occurs at about the time the reaction to the coccidioidin skin test becomes positive.
It may be the only symptom and indicates a good prognosis. Before this time, some patients (about 10%) develop a toxic erythema, usually in the first few days of
illness. The rash is a diffuse, fine, macular erythematous reaction covering the trunk and extremities and usually occurs in children with the disease.
Roentgen findings in symptomatic primary disease are those of air-space pneumonia, which results in homogeneous opacity that is poorly circumscribed and may be
segmental or lobar. It tends to involve the lower lobes and may be associated with some atelectasis. In other patients, there is patchy central disease that tends to
resolve quickly (in 1 to 2 weeks). Pleural involvement is found in about 20%, usually manifested by a minimal effusion. The hilar nodes are enlarged in about 20% of
these patients, usually on the side of the alveolar disease. The roentgen findings in this type of involvement simulate those of other acute, atypical pneumonias. The
pneumonia of coccidioidomycosis may be localized to one segment, but wider dissemination has also been reported, with multiple areas of pneumonic consolidation.
Occasionally, the adenopathy in the hilar and mediastinal nodes is the predominant feature, and in these patients there may or may not be evidence of pulmonary
parenchymal involvement. Multiple nodular parenchymal lesions have also been reported but are not as common as the more localized pneumonitis. Cavitation within
the area of disease is not uncommon. The cavities are usually small and may disappear quickly in the primary type of infection. Occasionally, small pleural effusion is
the only evidence of the disease noted on the chest roentgenogram. Although effusion occurs in about 20% of patients with coccidioidomycosis, pleuritic chest pain has
been reported in 70%. Massive effusion is rare and may result from direct spread of pulmonary disease across the pleural space.
Persistent pulmonary coccidioidomycosis is found in about 5% of patients. It is a much more significant type of disease and may be fatal. In these patients, coccidioidal
pneumonia may persist for months, with large areas of dense consolidation clearing very slowly. The patients are often very sick with persistent fever, prostration, chest
pain, productive cough, and occasional hemoptysis. This type of the disease usually occurs in susceptible patients and occasionally in immunosuppressed patients.
Cavitation, either thick- or thin-walled, may also occur and may be chronic. Bronchiectasis and bronchial stenosis are uncommon. 87
A more benign type of residual or persistent pulmonary coccidioidomycosis results when the acute primary disease subsides without much dissemination. The primary
disease may clear completely, but when there is residual disease, it usually assumes one of three general radiographic types: cavitation; nodules, which may be single
or multiple; or pulmonary opacity, which may be relatively focal and occur in a single area or in several areas. The residual type of cavitation in this form of
coccidioidomycosis often is thin-walled and may remain unchanged in size and shape for years. There usually is some fibrotic disease in the area of cavitation, but this
is not always true.
Studies of many patients have shown that the thin-walled cavity that was originally thought to be characteristic of the disease occurs in only 50% to 60% of patients,
and the remaining cavities have relatively thick walls. Spontaneous closure of cavities occurs in about one half of the patients. Most of the cavities are single and in the
upper lung, and more than half are 4 cm or less in diameter. Cavitation may be complicated by secondary infection, including formation of Aspergillus fungus balls,
pyopneumothorax when the cavity is subpleural in location, or pulmonary hemorrhage, which usually is not significant. These complications are uncommon. Cavitation
in coccidioidomycosis must be differentiated from that in pulmonary TB and other mycotic infections. This usually is not possible on roentgen evidence alone, but as a
general rule the residual cavity in coccidioidomycosis has less pulmonary disease around it than is seen in untreated pulmonary TB, because bronchogenic spread is
much less common. This finding is important in the differential diagnosis of untreated patients with chronic pulmonary disease in whom there is persistent cavitation
(Fig. 24-49).

 Rarely, a pulmonary mycetoma (fungus ball) may be caused by C. immitis.109 Arthrospores and spherules may
be present along with hyphae of the mycelial phase in a pulmonary cavity. The appearance is similar to that of
an aspergilloma, a much more common cause of fungus ball.
The nodular residuals of coccidioidomycosis vary considerably in size and number. They may or may not contain
calcium. When single, they must be differentiated from those of other diseases that cause solitary pulmonary
nodulation, including primary bronchogenic tumor. When multiple, the lesions must be distinguished from other
mycotic disease and from pulmonary TB. These differentiations are not possible on roentgen examination and
must be based on skin tests with coccidioidin and serologic studies. The infiltrative fibrotic type of residual
disease is similar to the fibrotic residues of numerous other inflammations, so there is nothing in the
roentgenogram to indicate the nature of the original disease. Pleural thickening and effusion are occasionally
noted as the end results of this disease, but there is nothing characteristic about these findings. Cavities are
often peripheral and tend to rupture into the pleural space, resulting in empyema. Occasionally, they cause
spontaneous pneumothorax.
Disseminated coccidioidomycosis occurs rarely when the initial infection fails to become localized. This is very
uncommon in whites, but members of dark-skinned races are more susceptible. Clinically, dissemination is a
continuation and progression of the primary infection, is often manifested by exacerbation of symptoms, and
may result in acute respiratory failure. Occasionally, an acute form of the disease may progress rapidly and
disseminate widely. Although the miliary spread usually occurs early in the disease, it is sometimes a late
complication of chronic pulmonary or extrapulmonary forms. Radiographic findings vary considerably, from
universal hematogenous spread of disease resembling miliary TB to local spread confined to the lungs. There is
often bronchogenic dissemination to the opposite lung or other lobes, which results in scattered involvement of
varying extent. Large cavities may appear, along with pleural involvement leading to empyema. Associated with
the extensive pulmonary opacities in this form of the disease, there is often spread to abdominal viscera, the
skeletal system, lymph nodes, and sometimes the brain and meninges. The disseminated type of involvement is
usually lethal.

Coccidioidomycosis.
A: Note the cavity in
the left subclavicular
area. The elongated
cavity
has
a
moderately
thick
wall, but there is very
little
parenchymal
disease around it. B:
One year later, the
cavity is larger, the
wall is thinner, and
again very little other
parenchymal disease
is observed.

 Rarely, a pulmonary mycetoma (fungus ball) may be caused by C. immitis.109 Arthrospores and spherules may be present along with hyphae of the
mycelial phase in a
pulmonary cavity. The appearance is similar to that of an aspergilloma, a much more common cause of fungus ball.
The nodular residuals of coccidioidomycosis vary considerably in size and number. They may or may not contain calcium. When single, they must be
differentiated
from those of other diseases that cause solitary pulmonary nodulation, including primary bronchogenic tumor. When multiple, the lesions must be
distinguished from
other mycotic disease and from pulmonary TB. These differentiations are not possible on roentgen examination and must be based on skin tests with
coccidioidin and
serologic studies. The infiltrative fibrotic type of residual disease is similar to the fibrotic residues of numerous other inflammations, so there is
nothing in the
roentgenogram to indicate the nature of the original disease. Pleural thickening and effusion are occasionally noted as the end results of this
disease, but there is
nothing characteristic about these findings. Cavities are often peripheral and tend to rupture into the pleural space, resulting in empyema.
Occasionally, they cause
spontaneous pneumothorax.
Disseminated coccidioidomycosis occurs rarely when the initial infection fails to become localized. This is very uncommon in whites, but members of
dark-skinned
races are more susceptible. Clinically, dissemination is a continuation and progression of the primary infection, is often manifested by exacerbation
of symptoms, and
may result in acute respiratory failure. Occasionally, an acute form of the disease may progress rapidly and disseminate widely. Although the miliary
spread usually
occurs early in the disease, it is sometimes a late complication of chronic pulmonary or extrapulmonary forms. Radiographic findings vary
considerably, from universal
hematogenous spread of disease resembling miliary TB to local spread confined to the lungs. There is often bronchogenic dissemination to the
opposite lung or other
lobes, which results in scattered involvement of varying extent. Large cavities may appear, along with pleural involvement leading to empyema.
Associated with the
extensive pulmonary opacities in this form of the disease, there is often spread to abdominal viscera, the skeletal system, lymph nodes, and
sometimes the brain and
meninges. The disseminated type of involvement is usually lethal.

Histoplasmosis
Histoplasmosis is caused by the fungus Histoplasma capsulatum.40 It was originally thought to be a rare
and fatal disease, but it is now known that the disseminated
form, which may be fatal, is only one of several types of the disease. The primary form is much more
common and is by far the most common fungal disease in the
United States. It is endemic in the Mississippi, St. Lawrence, and Ohio river valleys and along the
Appalachian Mountains. 86 In many areas, histoplasmin skin
sensitivity indicating previous infection is almost universal in young adult lifetime residents. The disease is
less common elsewhere in the United States but is found in
almost all states, as well as in Mexico and Panama.
The primary form of histoplasmosis, a localized pneumonic disease, is usually relatively benign and passes
unnoticed in most instances (95%). The roentgen changes
found in acute benign disease are varied, with single or multiple areas of pneumonic consolidation. The
disease cannot be distinguished from primary TB
roentgenographically. It is often segmental in distribution and may be accompanied by hilar node
enlargement. The hilar node involvement may be more prominent
than the parenchymal disease in some subjects (Fig. 24-50), particularly children. In addition to the
localized pneumonic consolidation, there is a more disseminated
form, which often occurs in local epidemics. Poorly defined, patchy or nodular lesions are scattered
throughout both lungs ( Fig. 24-51 and Fig. 24-52). Later they
become more clearly defined, round nodules varying in size up to 1 cm. With healing, some of the nodules
may disappear completely, whereas others may gradually
decrease in size and become calcified ( Fig. 24-53). Calcification often occurs in the involved hilar nodes as
well.

 Histoplasmosis is the most common cause of broncholithiasis, which is produced

when a calcified node erodes into a bronchus. Studies of large groups of people in
endemic areas have shown that, as a general rule, the amount of calcification in
parenchymal nodules and in hilar nodes is greater in histoplasmosis than in TB. The
primary form of the disease may clear and leave no pulmonary residuals that can be
recognized on roentgenograms. In other cases, a solitary calcified parenchymal
nodule with or without calcified hilar nodes may be present ( Fig. 24-54). Caseous
lymphadenitis is common during the primary infection ( Fig. 24-55; see Fig. 24-52).
Cyst-like lesions may develop in the mediastinum and become very large when
liquefaction occurs in enlarged coalescent nodes. These lesions can measure 10 cm
or more in diameter and may be asymptomatic. Airfluid levels can develop within
them when there is communication with the bronchial tree or lung. Remnants of
lymph node tissue may be observed in these cyst-like lesions, which tends to confirm
the impression that they represent excavated lymph nodes. Miliary parenchymal
calcifications scattered throughout the lungs and large mulberry calcified hilar
nodes are usually associated with histoplasmin sensitivity rather than tuberculin
sensitivity.

 Symptomatic primary infection is usually found in infants and young children. In contrast to patients with the more benign
common form, these patients usually have a cough and are often febrile for a few days, or occasionally for 2 to 3 weeks or
longer. Roentgen findings consist of hilar and mediastinal adenopathy with a focal opacity representing air-space disease in
the lung. Nodes may calcify and occasionally may obstruct a bronchus or rupture into it.
The acute epidemic form of histoplasmosis reported in several localities in the endemic regions probably represents a heavy
exposure that results in more pulmonary parenchymal involvement than in the usual primary form of the disease. Extensive
bilateral lobular or nodular air-space disease may involve both lungs, and sometimes a miliary spread throughout both lungs
is observed. The residuals are similar to those of the benign primary form, except that there may be more scattered, calcific,
parenchymal foci in the severe acute epidemic form. It appears that reinfection may produce the acute, chronic, or
disseminated form of histoplasmosis.
Disseminated histoplasmosis is a progressive disease with dissemination not only to the lungs but also to other organs,
including the bone marrow. The course may be extremely rapid and fulminating or slowly progressive, leading to cachexia
and anemia. It usually occurs in infants, in patients with compromised cellular immunity, or in those who have been
immunosuppressed. Marked variation has been found in the roentgen manifestations of disseminated pulmonary
histoplasmosis, ranging from widespread granular nodulations throughout both lungs (the most common finding) to a lobar
type of pneumonic consolidation. Scattered involvement simulating other types of pneumonia may also be noted, and
occasionally there is massive pleural effusion. In infants younger than 1 year of age the acute disseminated form is often
fatal; hepatosplenomegaly is common in addition to the extensive pulmonary involvement.
There is an intermediate form of histoplasmosis that results in chronic active fibrocavitary pulmonary disease resembling
reinfection TB clinically and radiographically.
Cavitation along with local ill-defined opacities and nodulation similar to that seen in chronic pulmonary TB is often found.
Pleural involvement, fibrosis, and contraction of the involved lobe or segment with alteration in the size of the thorax and
mediastinal deviation may also be produced ( Fig. 24-56). Histoplasmosis involving hilar nodes adjacent to bronchi may
cause collapse of the middle lobe (middle lobe syndrome) or of other pulmonary segments. It may also be the cause of
broncholithiasis. In patients with chronic active pulmonary histoplasmosis, the apical posterior segments are involved and
cavitation is common, often persisting for long periods. These persistent cavities often enlarge gradually and may become
very large. Disease in the adjacent lung is common, and fibrosis may become extensive.

Histoplasmosis. The
parenchymal
disease is minor
and consists of a
small amount of
patchy opacity
above the right
hilum; there is
bilateral hilar node
enlargement, more
on the right than on
the left.

Disseminated
pulmonary
histoplasmosis. Note the small,
poorly defined nodules scattered
throughout the left lung. The
patient had been ill for several
weeks.

A and B: Histoplasmosis. Computed tomogram shows a cavitating

nodule in the right upper lobe and mediastinal adenopathy caused by
histoplasmosis infection.

Histoplasmosis.
Examples
of
calcified pulmonary
nodules.
A:
The
nodules seen here
are rather uniform
in size, and all are
calcified. B: Fewer
nodules but less
calcification
and
more variation in
size are noted in
this patient.

Histoplasmosis. There is
a
solitary,
partially
calcified
parenchymal
nodule in the right
upper lung with several
partially calcified right
hilar nodes. The left
hilum is also prominent;
enlarged nodes appear
there.

Histoplasmosis.
There
are enlarged nodes in
the left hilum and some
parenchymal disease in
the lung lateral to the
hilum, which appears
somewhat nodular. No
other
disease
was
observed.

Histoplasmosis. Note the

conglomerate disease in
the central and basal lung.
There is also some pleural
thickening and a small
amount of fluid. No definite
hilar enlargement is
present. This is the same
patient whose
roentgenogram, obtained 5
years before this study, is
shown in FIG. 24-55. Slow
progression of disease as
illustrated here is unusual
in our experience.

 Mediastinal involvement by histoplasmosis can result in fibrosing mediastinitis, a

progressive fibrotic process that entraps, encases, and narrows mediastinal
structures such as the superior vena cava, the pulmonary arteries and veins, and the
central airways ( Fig. 24-57).79,86 The fibrosis may be either localized
(mediastinal granuloma) or diffuse (fibrosing mediastinitis). 45 The primary disease may
have been asymptomatic, but the resultant fibrosing mediastinitis can produce
pulmonary arterial and venous obstruction, central lymphatic obstruction, pericardial
involvement, and esophageal involvement in addition to superior vena caval
obstruction. Most cases of fibrosing mediastinitis are now thought to be caused by an
abnormal, hyper-reactive fibrotic response to H. capsulatum antigens.45,86 Viable
fungal organisms are rarely recovered or grown from mediastinal tissue samples
obtained from patients with fibrosing mediastinitis. 45 Both CT and MRI can be used to
evaluate the extent of mediastinal fibrosis more effectively than conventional chest films.
On MRI, fibrosing mediastinitis appears as abnormal soft tissue infiltrating
the mediastinum with relatively low signal intensity on all pulse sequences ( Fig. 24-57).
On CT, calcifications within the infiltrating soft tissue may help differentiate
this condition from infiltrating lymphoma or carcinoma.86 Effective therapy for fibrosing
mediastinitis does not exist, and surgical palliation is of limited or no value.
Rarely, calcification of the pericardium may result from Histoplasma pericarditis.

Evaluation
of
fibrosing
mediastinitis
by
magnetic resonance
imaging.
T1weighted
coronal
( A) and axial (B)
and
T2-weighted
axial (C) images
show
low-signalintensity
fibrotic
material
encasing
the
airways
and
obliterating the right
pulmonary artery.

 In some cases, the sole manifestation of disease is a solitary pulmonary nodule,

the histoplasmoma. This lesion may be associated with calcified hilar nodes, and
there may be a few satellite nodules in the lung. Calcification may or may not be
present in the lesion, which varies from 1 to 3 cm or more in diameter. The
calcification may be laminated, annular, solid, or stippled, and it may be central
with a laminated or annular peripheral ring. The vast majority remain stable for
years,
but occasionally a slow increase in size is observed, suggesting that some
histoplasmomas contain viable organisms although most lesions are quiescent.
Skin
testing, complement-fixation studies, and mycologic studies are required to
differentiate this disease from pulmonary TB; occasionally, both diseases are
present in
the same patient. When the nodule does not contain calcium, it cannot be
differentiated from neoplasm on chest radiography, tomography, or CT; in such
cases,
biopsy may be necessary.

Cryptococcosis
Cryptococcosis (torulosis) is caused by Cryptococcus neoformans. Pulmonary lesions have been reported in increasing numbers of patients
with and without
involvement of the central nervous system. As in other chronic pulmonary infections, several forms of pulmonary involvement are found and
the diagnosis cannot be
made from roentgenograms alone.32,60 Three general types of radiographic change have been described. The first is a fairly well
circumscribed, round mass or nodule
usually occurring in the lower half of either lung, which must be differentiated from neoplasm and from other chronic pulmonary granulomas.
They tend to be
peripheral and may become large (up to 10 cm in diameter). At times, multiple, closely grouped, mass-like densities may be observed. The
second form is a
pneumonic type of lesion consisting of a somewhat irregular opacity more likely to appear in the lower than in the upper lobe. It represents
granulomatous disease. 32
This type of disease may be extensive but usually is confined to one segment or lobe and often is associated with lymph node enlargement;
cavitation is rare. This is
the most common form. The third type is a widespread miliary variety of nodulation, often found in conjunction with severe central nervous
system infection. This type
of disease is frequently found as an opportunistic infection associated with such chronic processes as Hodgkin's disease, leukemia, and
lymphoma; in patients who
have received steroid or antibiotic therapy; or as a complication of AIDS. Cavitation may occur in this form; pleural involvement with effusion
may be present but is
uncommon. Often the diagnosis is not made until autopsy in patients having disseminated disease.
In seven patients with AIDS complicated by cryptococcosis, Miller and associates 92 found that hilar or mediastinal adenopathy and interstitial
pulmonary disease,
alone or in combination, were the most common findings on chest films. They believe that the interstitial process is a manifestation of
disseminated disease and its
presence should initiate a search for silent cryptococcal meningitis. Although the diagnosis cannot be made on the basis of roentgenographic
findings, the
combination of signs of meningeal irritation and pulmonary lesions resembling those described is suggestive. When the disease is confined to
the lung in a
noncompromised host, spontaneous resolution without treatment occurs in most cases.

North American Blastomycosis

North American blastomycosis is caused by the yeast-like fungus Blastomyces dermatitidis. Although much less common
than histoplasmosis, it occurs in
approximately the same geographic areas of the United States but extends more eastward and northward. There are two
general types, cutaneous and disseminated.
In the disseminated form, the portal of entry is usually the respiratory tract, and 95% of the patients have some form of
pulmonary involvement. The roentgen findings
in pulmonary disease produced by this organism are not diagnostic and are related to the clinical form of the disease. 111 In
the acute form, there are four major
roentgenographic patterns. (1) Air-space involvement causing a patchy segmental or lobar consolidation is present in most
patients. There are often several foci of
disease, and involvement may be multilobar. The disease is usually located in the upper lung. In this type, resolution usually
takes place slowly and may require
several months. Cavitation may complicate this acute form. (2) A large, round, tumor-like mass or masses may be present
and may cavitate. (3) An extensive
reticulonodular or miliary interstitial pattern may be present. (4) A severe form of acute disease may occur in which there is
bilateral exudate with the distribution
resembling that of pulmonary alveolar edema. The onset is rapid, and the condition is very toxic in these patients. Several
patients have developed ARDS as a result
of this severe disease; this combination is usually fatal.
The chronic form of the blastomycosis in the upper lobe resembles pulmonary TB. In the most common form, there is a
fibronodular appearance consisting of
pulmonary nodules and linear fibrotic strands ( Fig. 24-58, Fig. 24-59, and Fig. 24-60). Only slightly less common is cavitary
upper-lobe disease in which the walls are
moderately thick and smooth. Much less common is a mass-like appearance, which can closely resemble bronchogenic
carcinoma ( Fig. 24-60). The disease may
extend to the pleura, cross interlobar fissures, invade the chest wall, and cause rib destruction, but not as frequently as
actinomycosis.

North American blastomycosis.

Note the extensive disease in the
right parahilar and medial basal
areas as well as in the central and
right lung laterally. Adjacent to the
dense homogeneous involvement,
several scattered, poorly defined
nodules
are
observed.
Roentgenographic findings in this
disease are nonspecific.

North American blastomycosis.

Numerous
disseminated
nodules, ranging up to 1 cm or
more
in
diameter,
are
observed. On the right, either
dense disease overlies the
hilum or adenopathy is present,
but no adenopathy is noted on
the left.

Blastomycosis. Chest film (A) and computed tomogram (B)

show a large, mass-like consolidation in the left upper lobe
plus multiple nodules in the opposite lung. The mass-like
appearance of these opacities could be mistaken for a lung
neoplasm with metastases.

 Chest radiographic findings in 63 patients reported by Sheflin and colleagues 120

showed single upper-lobe involvement in 27 patients and multilobar disease in
21. In
nine patients, the major abnormality was a pulmonary mass. Pleural effusion
and/or adenopathy (hilar or mediastinal) was present in 20%. Cavitation was
found in 23
patients. Five patients had diffuse disease, and only one had a miliary type of
disease.
Blastomycosis is unusual in children except in small epidemics, which have been
reported on several occasions. Children develop alveolar disease, with multiple
small, thin-walled cavities in about 25% of cases. Hilar adenopathy may also be
present, and pleural effusion is not unusual. If children develop the disseminated
form, it may be fulminant with a high mortality rate. Because these changes are
similar to those noted in pulmonary TB, mycotic infections, and other chronic
inflammatory diseases as well as neoplasm, the diagnosis must be based on
mycologic studies.

South American Blastomycosis

(Paracoccidioidomycosis)
This disease, caused by Blastomyces brasiliensis, is
found most commonly in Brazil but has also been
reported in the other South American countries.
Pulmonary
involvement is said to occur in 80% of patients with the
visceral type of disease. The portal of entry may be the
intestinal tract in this disease; the pulmonary lesions
are secondary and are widespread and nodular in type,
often associated with hilar adenopathy. The disease
may also manifest as a cavitary pulmonary mass. 1
Destructive bone lesions are common in the
disseminated form.

Pulmonary Aspergillosis
Aspergillus species are ubiquitous and cause a wide spectrum of pulmonary diseases.
These include asymptomatic saprophytic colonization of the airways or
pre-existing cavities (aspergillomas), ABPA, semi-invasive (chronic necrotizing)
aspergillosis, and invasive pulmonary aspergillosis. 38 Aspergillus infections have also
been categorized as primary or secondary. Most often, Aspergillus infection is a
secondary process in patients who have been treated with antibiotics and in those
with debilitating disease. However, it occurs rarely as a primary disease in otherwise
healthy persons.
Two clinical and roentgen types of the primary disease have been described. The first is
an acute bronchopneumonic form with scattered multiple areas of pneumonic
consolidation, some of which break down to form cavities. This disease may progress
with severe invasive destructive pulmonary disease eventually leading to death.
The invasive form is usually seen in infants. There is often enough hilar node
enlargement to be recognized as such on the roentgenograms. The second type of
primary disease is more chronic and milder. Irregular and rounded nodular opacities
closely resembling those seen in pulmonary TB are present. The clinical course
of this disease is less severe than that of TB; the diagnosis must be made on the basis of
identification of the organism in the sputum, often with some reservation
because the organism is so commonly found there.

Secondary Aspergillosis
Secondary aspergillosis is found in three classic forms, the
aspergilloma (mycetoma or fungus ball), ABPA, and a severe
life-threatening form (invasive pulmonary
aspergillosis), which usually is found in patients with severe
immunosuppression and neutropenia from aplasia-producing
cytotoxic drugs, steroids, or other
immunosuppressive agents. More recently, a more indolent
form of Aspergillus infection has been recognized. Semiinvasive aspergillosis or chronic necrotizing
aspergillosis is less aggressive than invasive pulmonary
aspergillosis and occurs in milder forms of immunosuppression,
often in patients who have underlying lung
disease (i.e., patients with alcoholism, chronic debilitating
disease, COPD, sarcoidosis). 38

Invasive Pulmonary
Aspergillosis
Invasive pulmonary aspergillosis can develop in immunocompromised patients and,
rarely, in immunocompetent patients. Patients with acute leukemia and
granulocytopenia are particularly susceptible. Occasionally it occurs as a complication of
influenza-like viral infections in the noncompromised host. It may be
associated with other infections; mucormycosis appears to be the most common of
these.77
The radiographic changes are quite variable. Air-space disease in the form of round
pneumonia resembling a poorly defined mass, single or multiple, seems to be a
common finding. Many of these lesions eventually cavitate, and some are probably
hemorrhagic pulmonary infarcts ( Fig. 24-61). The latter results when the organism
invades and obstructs a branch of the pulmonary artery. Some of the cavitations exhibit
an air-crescent sign, caused by a mass within the cavity, that does not move
with a change in the position of the patient and probably represents necrotic tissue in an
area of infarction. A diffuse bronchopneumonia pattern may develop at any
time. This may progress to extensive bilateral pulmonary involvement. Chest wall
invasion can occur, with bone destruction, but is not common. If this is complicated
by empyema, the prognosis is poor. Rarely, a miliary spread throughout the lung is
observed. In these patients the prognosis is also poor, and the immediate cause of
death may be aspergillosis. Because the or

A and B: Computed tomographic (CT) scans of a 22-year-old man with acute

myelogenous leukemia undergoing chemotherapy and severely neutropenic with fever.
CT demonstrates the typical features of invasive pulmonary aspergillosis in this patient
population. Two inflammatory masses are seen, each with a surrounding CT halo of
ground-glass opacity around the denser center of the mass. Invasive pulmonary
aspergillosis invades pulmonary blood vessels, causing hemorrhagic infarction, and the
CT halo corresponds to hemorrhage and edema around the focus of fungal infection.

 The CT appearance of invasive pulmonary aspergillosis can be quite characteristic

early in the course of the infection ( Fig. 24-61). CT may show one or more nodules
or masses with the CT halo sign, a surrounding zone of ground-glass opacity which
results from pulmonary hemorrhage around the focus of infection and infarction
caused by the angioinvasive aspergillus organism. 66 This is a feature of early invasive
pulmonary aspergillosis and precedes cavitation of the nodules on plain films
or CT. CT is more accurate than chest radiography in detecting early lesions of
invasive pulmonary aspergillosis. The use of CT in the evaluation of the neutropenic
patient is discussed in Chapter 25.
Sometimes the invasive form of the infection invades the airways rather than the
blood vessels. This has been called invasive aspergillosis of the airways or
necrotizing aspergillus tracheobronchitis. Like the angioinvasive form of the infection,
the invasive airway disease occurs usually in severely immunocompromised
patients, but it is much less common than the angioinvasive form. CT findings may
include lobar consolidation, peribronchial consolidation, centrilobular nodules,
tree-in-bud opacities, and, less commonly, diffuse bronchiectasis indicative of an
infectious bronchitis and bronchiolitis. 80

Semi-invasive or Chronic
Necrotizing Pulmonary Aspergillosis
This form of the infection usually occurs in patients with milder forms of
immunosuppression, often in conjunction with underlying lung disease.
Among those at risk
are patients with sarcoid, diabetes mellitus, COPD, alcoholism, or
malnutrition ( Fig. 24-62). Corticosteroid therapy and prior radiation
treatment are also predisposing
factors.38 As the name implies, semi-invasive aspergillosis is more
indolent and chronic than invasive pulmonary aspergillosis. It typically
is more localized, usually
begins in an upper lobe or lung apex, and slowly progresses. Its
appearance often mimics that of reactivation TB. 38 Consolidation and
then cavitation gradually
progress over the course of weeks to months. Exuberant adjacent
pleural reaction is a common associated feature, and infection may
extend to chest wall or
mediastinal invasion38

A and B: Semi-invasive pulmonary aspergillosis. This elderly man with

chronic obstructive pulmonary disease developed a progressive rightupper-lobe pneumonia as the result of aspergillus infection. Computed
tomography nicely demonstrates the patient's extensive emphysema
and the extent of the necrotizing pneumonia.

Mycetoma (Aspergilloma)
The aspergilloma (mycetoma) or fungus ball consists of a localized round or ovoid mass made up of
Aspergillus hyphae (the mycelial form), blood, cellular debris,
fibrin, and mucus that occupies a cavity slightly larger than the mass. This is a saprophytic,
noninvasive colonization of a pre-existing cavity by Aspergillus
organisms.38 The cavities and fungus balls are usually found in the upper lobe, probably because
the primary disease that causes the underlying cavity, commonly TB
or sarcoidosis, occurs in the upper lobe. A thin, radiolucent rim is observed surrounding the mass.
This is caused by air in the space between the thin cavity wall and
the mass and is referred to as the air-crescent sign or Monod's sign. 38 Air-crescent formation is also
seen in invasive pulmonary aspergillosis, but the pathophysiology
is different: in the invasive form, pulmonary infarction and cavitation are caused by the invasive
fungal infection, but in the noninvasive aspergilloma the intracavitary
mass usually moves within the cavity. This can be demonstrated on CT by imaging in the supine and
prone positions. CT is often helpful in detecting and diagnosing
mycetomas, particularly when there is extensive underlying lung disease that makes the plain film
difficult to interpret ( Fig. 24-63). Calcification may occur within the
mass and may be extensive. Hemorrhage is common, often recurrent, and can be severe and lifethreatening. There may be no other symptoms, or the patient may
have mild constitutional symptoms of weight loss and fatigue.
Rarely, other organisms can form fungus balls. Candida species, C. immitis, Monosporium,
Sporotrichum, and Trichophyton species, among others, have been
implicated.38 About 10% of mycetomas undergo spontaneous lysis.

A and B: Aspergilloma. This 37-year-old Tibetan monk had a history of

surgery in the right lung apex for tuberculosis. A small residual apical space
remained after surgery, and years later a fungus ball developed within it.

Allergic (Hypersensitivity)
Bronchopulmonary Aspergillosis
ABPA is seen in patients with chronic bronchial asthma and is caused by a hypersensitivity reaction to
antigens of species of the genus Aspergillus, chiefly
Aspergillus fumigatus.81 Both type I and type III hypersensitivity reactions are present in this disorder.
Serum immunoglobulin E is elevated, and immunoglobulin G
precipitins to Aspergillus antigens are present. The presence of peripheral blood and often lung-tissue
eosinophilia is characteristic, as is positive immediate skin-test
reactivity to Aspergillus antigens.38,129 The organisms colonize the airways and are sometimes found in
the sputum during an initial asthmatic attack or early in the
course of bronchial asthma. The patients usually have wheezing, fever, cough, and mucopurulent sputum,
often with expectoration of mucus plugs. A history of
asthma refractory to standard bronchodilator treatments is often elicited.
The roentgenographic findings can be divided into transient and permanent shadows 65 (Fig. 24-64).
Transient shadows are of several types. (1) Homogeneous
consolidation may be present and may be large or small without loss of volume. These lesions may be
massive, often are multiple, and tend to be central in location.
(2) A nonhomogeneous shadow or patchy consolidation may be present. (3) Small, circular, or nodular
shadows may be present. (4) Transient atelectasis of a
segment, lobe, or lung may be present. (5) Band-like and gloved-finger shadows 2 to 3 cm long and 5 to 8
mm wide may be present; at times they have a rounded
end, caused by mucoid impaction. (6) Two parallel hairline shadows may be present, with a radiolucent
zone between the lines representing a normal bronchus (tram
line). (7) A well-outlined, circular (ring) shadow with a diameter of 2 to 3 cm, also representing a bronchus,
may be present.

AC:
Allergic
bronchopulmonary
aspergillosis (ABPA). Roentgenographic and
computed
tomographic
(CT)
images
demonstrate central bronchiectasis, a
characteristic feature of ABPA. The CT also
shows some mucoid impaction in the left
lower lobe ( B).

 The permanent shadows include the following: (1) parallel lines similar to tram lines but with a width larger than that of a normal bronchus; (2)
hairline ring shadow 1
to 2 cm in diameter; (3) decreased volume but with aeration in the segment or lobe involved; (4) narrowing or loss of vascular shadows; and
(5) long-line shadows.
Most patients progress to varying degrees of pulmonary overinflation, some develop areas of fibrosis, and others have small areas of
atelectasis (segmental or less)
that may persist. Pleural effusion is rare but may appear. Bronchocentric granulomatosis with severe bronchial necrosis and granuloma
formation appears to be a
variant. The toothpaste and gloved-finger shadows represent mucus plugs or impactions in most instances. Occasionally, mucoid impaction
may occur in asthmatics
without aspergillosis. The tram-line shadows represent bronchi that are normal in diameter, whereas parallel-line shadows represent bronchi
that are increased in
diameter. The ring shadow represents a dilated bronchus observed on end. The latter two findings indicate bronchiectasis, which is usually
central and becomes
permanent if the patient is not treated promptly. Long-line shadows probably represent a wall of a bulla in some instances and pleura in others.
The diagnosis is made
on the basis of a history of bronchial asthma, the presence of eosinophilia, and the changing roentgenographic pattern of the lungs as
described. This disease usually
responds quickly to corticosteroid therapy.
The CT hallmark of ABPA is prominent, central or proximal bronchiectasis. Central bronchiectasis is so characteristic that if it is identified on CT
in a patient with
asthma or wheezing, the diagnosis of ABPA should be suggested. Areas of mucous plugging are very apparent on CT as well (see Fig. 24-64).
In addition to asthmatics, patients with cystic fibrosis are susceptible. The complication of bronchopulmonary aspergillosis appears to be a
major factor when these
patients deteriorate rapidly, so prompt treatment is important. If it is important to outline the bronchi for detection of bronchiectasis as well as
extent of the pulmonary
involvement, CT is very helpful in evaluation of this disease. Bronchial wall thickening and bronchiectasis are usually clearly defined.
Bronchocentric granulomatosis is now thought to represent a variant of ABPA in which a more localized Aspergillus infection produces
granulomatous inflammation
and disruption centered on the bronchioles. It occurs in young asthma patients. 129

Moniliasis (Candidiasis)
Candida (Monilia) albicans is a yeast-like organism, frequently present in the normal mouth, that is
usually saprophytic but occasionally mildly pathogenic for humans.
Because the organism is often present in normal people, it is difficult to document this disease.
The literature is very confusing, and many reported cases are probably
examples of other diseases. However, most investigators agree that Monilia can produce
bronchopulmonary disease, particularly in elderly or debilitated persons,
immunocompromised hosts, and infants. It is therefore an opportunistic organism that can produce
disseminated fatal disease in susceptible subjects. Roentgen
findings consist of a rather fine, mottled type of nodulation ranging from 2 mm to 1 cm in diameter
associated with some prominence of pulmonary markings or, more
commonly, segmental homogeneous consolidation. It can also produce a diffuse
bronchopneumonia pattern that may be bilateral.
Segmental or lobar air-space pneumonia has also been described. In infants, it can be a fatal
disease, with progressive alveolar consolidation and occasional
cavitation. It also can be widely disseminated to other organs as well as the lungs. Cavitation, with
or without a mycetoma, is rare but is simulated when the disease
involves an area of lung in which there are pre-existing emphysematous bullae. There may be
some enlargement of the hilar nodes. As with the other fungal diseases,
the diagnosis must rest on identification of the organism. Bronchial secretions should be
examined, rather than sputum, because the organism is a normal inhabitant
of the mouth.

Geotrichosis
Geotrichum candidum is a fungus frequently found in the mouth and gastrointestinal tract of
healthy subjects; it occasionally becomes pathogenic and causes
pulmonary as well as skin and mucous membrane infection. Pulmonary manifestations of
geotrichosis are not characteristic. Irregular, patchy densities are noted,
often in the upper lungs. Cavitation may develop, the cavities having rather thin walls.
Enlargement of the hilar nodes is frequent. The disease may closely resemble
pulmonary TB (Fig. 24-65). Geotrichum has a tendency to produce an opportunistic type of
pulmonary disease in severely debilitated or immunosuppressed patients.
In these patients, bronchopulmonary involvement is often extensive, with air-space disease
resembling extensive bronchopneumonia; often the infection is fatal.
Endobronchial disease, with positive sputum cultures and no pulmonary involvement visible
on chest films, may also occur in these patients. The diagnosis is based
on a positive skin test plus demonstration of the organism on repeated sputum examination.
Other fungal infections and TB must be excluded by appropriate studies,
because, as in moniliasis, the organism may be saprophytic rather than pathogenic.

Geotrichosis. Note the

nodular disease in the
left upper portion of the
lung, which resembles
pulmonary tuberculosis.
Since
the
disease
progressed
slowly,
resection
was
done,
proving
it
to
be
geotrichosis.

Other Mycoses
Sporotrichosis
Sporotrichosis, produced by Sporotrichum schenckii, usually involves
the skin, mucous membranes, and lymphatics. Rarely, pulmonary
infection is the primary
manifestation of the disease, presumably caused by inhalation of
spores. Most reported cases have been in the Mississippi and Missouri
river valleys. 105 Of all
reported cases, 40% have been in alcoholics. There is nothing
characteristic about the pneumonia it produces. 88 However, cavitation,
which may be bilateral, is often
observed, usually in upper lobes. The pulmonary infection may be local,
indolent, and granulomatous and resemble chronic pulmonary TB, or it
may be suppurative
and produce foci of bronchopneumonia. Scattered hematogenous smallnodular disease is rare, but hilar adenopathy is common. S. schenckii is
sometimes found as
a secondary invader in patients with chronic pulmonary TB.

Penicilliosis
Fungi of the genus Penicillium are
capable of producing a pulmonary
infection known as penicilliosis. This
disease is very rare. The fungus can
cause lung abscess
that cannot be distinguished from
cavitation produced by other organisms;
there are no roentgen signs that would
lead to the specific diagnosis.

Mucormycosis (Phycomycosis)
Mucor is a genus of fungus that is widely distributed in nature and not usually
pathogenic to humans. Along with Absidia and Rhizopus, it is a member of the
class
Phycomycetes. Several cases of severe disseminated infection caused by this
fungus have been reported in diabetics ( Fig. 24-66). This infection is also found
in
patients with other underlying debilitating disease, such as leukemia or
lymphoma, and in immunosuppressed patients. It is an opportunistic organism
found most
often in patients with hematologic disorders. In some of these, a widespread,
rapidly fatal confluent pneumonia that may cavitate is present. Like invasive
pulmonary
aspergillosis, mucormycosis is angioinvasive. The hyphae tend to invade and
occlude vessels, and the resultant infarction leads to the cavitation. The chest
film and
CT findings may therefore resemble those of invasive pulmonary aspergillosis.
In some instances, mucormycosis may be the cause of a solitary pulmonary
nodule.

Mucormycosis
infection in a diabetic
patient. A large thick
walled
cavity
is
present in the right
midlung
and
a
second mass in the
right lung apex.

DISEASES OF SPIROCHETAL ORIGIN

Syphilis
Involvement of the lungs in syphilis is very rare, but when it does occur it may simulate other chronic pulmonary diseases
symptomatically and radiographically. The diagnosis depends on exclusion of other diseases and on laboratory studies as
well as response to antiluetic therapy.
Three radiographic types of pulmonary involvement have been described. (1) Interstitial fibrosis may occur, resulting in
linear opacities radiating into the lungs from the hila. (2) A large, solitary mass (gumma) may be present. It may be clearly
circumscribed and resemble pulmonary tumor. Because some irregular inflammatory disease may surround it, the lesion can
simulate other types of inflammatory disease. 50 (3) Chronic lobar pneumonia may occur with fibrosis and decreased size of
the diseased lobe. This type resembles chronic pulmonary TB. Another chest film finding in patients with syphilitic aortitis is
the presence of extensive calcifications in the wall of a dilated ascending aorta, with ascending aortic disease occurring out
of proportion to, or in the absence of, calcification involving the descending aorta.
However, radiographic findings are not diagnostic, so serologic and histologic studies are necessary.
Leptospirosis
Leptospirosis is produced by a group of spirochetes called Leptospira. Four of more than 100 serogroups cause most of the
disease in humans. Several clinical forms have been described, and pulmonary involvement (in 20%) is only a part of
widespread disease in most instances. Occasionally, hemorrhagic pneumonitis is an early or striking manifestation.74
Three general types have been described. The most common (57% of 58 patients in one study 55) consists of widely
disseminated small areas of air-space consolidation representing hemorrhage and edema. The individual lesions are poorly
defined, with hazy nodules that resemble other acute, disseminated pulmonary inflammations. A second type of
leptospirosis (16%) is characterized by a large confluent area of consolidation similar to that found in lobar or segmental
pneumonia.
A third type (27%) consists of small, patchy densities that resemble bronchopneumonia or a more linear interstitial type of
disease, such as is noted in virus pneumonitis. Im and colleagues55 describe this type as having a diffuse ground-glass
appearance. Pleural effusion, often large, is common. Because the pneumonia is hemorrhage, it usually resolves within 2
weeks in patients who survive. The diagnosis cannot be made on the basis of roentgen findings and depends on
bacteriologic studies.

PROTOZOAN DISEASES

Amebiasis
Amebic infection of the thorax is usually secondary to gastrointestinal involvement, which follows the ingestion of the cysts of Entamoeba histolytica. It often is
associated with hepatic amebiasis. Rarely (fewer than 5% of cases), amebic lung abscess or ameboma is found without other signs or symptoms of amebiasis.
The roentgen signs are somewhat different in the two types of disease. In the pulmonary disease without hepatic abscess, parenchymal consolidation, often
complicated by abscess, develops well above the diaphragm. The abscess is similar to that produced by other organisms. When an abscess evacuates into a
bronchus, an airfluid level can be demonstrated in upright views. The abscess cavity may become very large, and associated pleural effusion is not uncommon.
When an ameboma without cavitation is present, it resembles any other lung mass and must be differentiated from other inflammatory masses and from tumor.
When the pulmonary disease or pleural disease is secondary to hepatic involvement, the appearance is somewhat more characteristic. The hepatic abscess causes
elevation of the diaphragm, and fluid in the right pleural space is common. The lower and middle lobes adjacent to the diaphragm are involved by a confluent
pneumonia in which cavitation may occur. In some instances the infection is confined to the pleural space, in which case an amebic empyema is formed; this is often
loculated at the base. In other instances, there is a combination of pleural and pulmonary involvement, with empyema and lung abscess. An amebic lung abscess may
rupture into a bronchus and drain spontaneously. Empyema must be drained if it does not rupture into the lung and drain spontaneously. Rarely, hepatic amebic
abscess may extend into the pericardium, resulting in amebic pericarditis. The diagnosis is confirmed by the presence of E. histolytica in the sputum or in the pleural
fluid.
Toxoplasmosis
Toxoplasmosis is caused by the protozoan parasite Toxoplasma gondii. The organism has an affinity for the central nervous system, the eyes, and the lungs. There is
an infantile form of the disease in which it is not uncommon to find cerebral involvement, beginning in utero, resulting in scattered intracranial calcifications in the
newborn. The disease behaves differently in the adult and involves the lungs primarily, rather than the central nervous system. The roentgen findings in the lungs are
similar to those noted in bronchopneumonia or viral pneumonia, namely air-space disease, often with some interstitial involvement. Enlargement of the hilar nodes is
frequently associated with the pulmonary involvement. Miliary dissemination produces opacities not unlike those noted in other acute miliary infections. If the disease
becomes chronic, it may result in scattered areas of fibrosis and in scattered nodules, some or all of which may become calcified.
Toxoplasmosis can also be an opportunistic disease involving the central nervous system and the lungs. Radiographic changes in the lung are variable. Widely
scattered, small, nodular or miliary densities have been described as the most common manifestation. In other cases there is focal air-space disease bilaterally, and
changes simulating interstitial pulmonary edema have also been described. The diagnosis can be made by serologic tests.

PLATYHELMINTH (FLATWORM)
INFESTATION
Echinococcosis (Hydatid Disease)
The small tapeworm, Echinococcus granulosus, is found in the intestinal tract of dogs. Its larval form is the cause of hydatid cysts.
The ova are ingested by humans
and migrate to the liver or lungs, where they produce a round or oval density that may become massive ( Fig. 24-67). Since the cyst
is readily molded as it grows, the
shape varies depending on its relation to the bony thorax. It appears on the roentgenogram as a round or oval, clearly defined,
dense mass that may produce some
adjacent atelectasis. A change in shape may be noted at fluoroscopy and with change in position of the patient. A wall, the pericyst,
is formed and is composed of an
external capsule produced by the host tissue. The hydatid cyst itself has a double wall composed of a thick outer membrane (the
exocyst) and a thin inner wall of
germinal cells (the endocyst). The cyst may rupture into a bronchus and empty part of its contents, in which case an airfluid level
is noted. This indicates separation
of the cyst from the host tissue capsule (pericyst). When this is observed, the roentgenographic diagnosis can be made with
reasonable certainty. The collapsed cyst
wall may float on the fluid surface and be outlined by air above it on an upright film (the water-lily, camalote, or iceberg sign). 15
This is virtually pathognomonic of
hydatid disease.
Rarely, rupture of the pericyst or host capsule leaves air between it and the exocyst. The crescent or meniscus sign, representing
radiolucent air between the cyst and
the host, may then be observed; it is a distinctive roentgen sign of hydatid cyst. Pulmonary cyst walls rarely calcify, in contrast to
the hepatic lesions, in which
calcification is common. When the cyst ruptures, there is a possibility of spread to other parts of the lung, giving rise to multiple,
small daughter cysts. Occasionally,
many small cysts are scattered throughout the lungs. Rarely, the cysts form in the pleural space or rupture into the pleural space
and cause pleural effusion. When
calcified hydatid cysts are present in the liver and a pulmonary cyst is detected, the diagnosis can be made with a considerable
degree of accuracy. 114

Echinococcal disease. A:
Computed tomogram (CT)
through
the
abdomen
demonstrates a large cyst
with daughter cysts in the
liver. Infection has broken
out through the liver
capsule and transgressed
the diaphragm; pockets of
infection are present in
the right lung base. B: A
more superior CT slice
demonstrates a nodule in
the
right
lung
apex
caused by dissemination
of the infection to the
lungs.

Cysticercosis
Occasionally, humans develop autoinfection when they ingest
eggs of the pork tapeworm, Taenia solium. The eggs emerge
as oncospheres in the gastrointestinal
tract, enter the bloodstream, and are carried to various organs
and tissues where they metamorphose into cysticerci. The
cysticerci may be found scattered widely
throughout the tissues, including the lungs, where they
produce scattered, soft-tissue nodular densities. When the
tapeworms die, calcification occurs and multiple
oval or spindle-shaped calcifications measuring about 3 by 10
mm can then be noted, scattered in the lungs and in other
tissues as well. The disease, cysticercosis, is
very rare in the United States but common in Africa, China,
and India.

Paragonimiasis
The lung fluke Paragonimus westermani is distributed widely in the Far East, particularly Korea, Taiwan, and Indonesia; in Africa; and in parts of
South
America.12,22,99,128 Humans are infested by eating undercooked crayfish or crabs or drinking infested water. The larval forms are liberated in the
jejunum and migrate
through the diaphragm and pleural space into the lung, where they mature into adult flukes, usually in the lower lobes. The disease is mild and
seldom fatal but does
produce symptoms in some patients. Hemoptysis is a frequent symptom of infestation, along with cough productive of brown or rusty sputum and
chest pain. In about
one third of those infested, the organism causes an ill-defined consolidation in the lower lung in the form of a hazy shadow of low, uneven density. In
about another
third, the density is more homogeneous, is more clearly defined, and may appear lobulated. Thin-walled, cyst-like cavitations may develop within the
area of
consolidation. Often the cavities are multiple and have a bubble-like appearance. In some patients, the disease is manifested by linear streaks that
appear within a
shadow of low-density consolidation. The involved area does not usually occupy a very large volume of the lung and may be unilateral or bilateral.
The basal and
peripheral midzone pulmonary disease is often not very conspicuous because of the small volume of lung involved and the low density of the
disease, which may
disappear completely. Pleural thickening in the interlobar fissures is also observed, and fleeting densities thought to represent Lffler's pneumonia
often accompany
the disease. Dense linear opacities are caused by burrows of the organism, which can be demonstrated by bronchography to be independent of
bronchi. The burrows
probably communicate with the cavities. Pleural effusion is common (in about 50%) and may be the only manifestation of the disease in some
patients.
Reports differ somewhat as to incidence of various findings. Suwanik and Harinsuta 128 found the following: (1) ring-like, cystic cavities with
crescent-shaped opacity
along one side ranging from 6 mm to 4 or 5 cm in 82%; (2) poorly defined nodular opacities up to 3 or 4 cm, usually basal or peripheral, in 48%; (3)
linear shadows at
bases, usually associated with ring-like shadows, in 21%; and (4) pleural thickening in 21%.
Calcification may develop, probably in dead parasites. Complications include empyema, bronchopleural fistula, and pulmonary cavitation. Ova may
be found in the
pleural fluid and in the sputum during the periods of hemoptysis. The disease may persist for many years.

Schistosomiasis
Schistosomiasis is caused by three blood flukes of the genus Schistosoma, S. mansoni, S. japonicum, and
S. haematobium. It is common in many parts of the world,
including Africa, Asia, and Puerto Rico, but is rarely if ever acquired in the United States. Pulmonary
disease is usually caused by S. mansoni or S. japonicum.
Several types of pulmonary reaction to the infestation may occur. As the larval forms pass through the
lungs, an apparent allergic response produces transient mottled
densities. Roentgen findings in this acute form consist of transient interstitial opacities, usually a fine
nodular pattern that may resemble miliary TB but clears
spontaneously without treatment.
Ova reach the lungs from the veins of the bladder, intestine, and liver. They may implant in or around
pulmonary arterioles, producing a necrotizing arteritis and
intra-arterial and periarterial granulomas, which result in a chronic pulmonary disease. Either of these
granulomas may obstruct the vessel. The organisms rarely
cause multiple arteriovenous fistulae.
Roentgen findings in the chronic form consist of central enlargement of pulmonary arteries secondary to
pulmonary hypertension and evidence of cor pulmonale,
which occurs in only 5% of patients with pulmonary disease. 82 More commonly, a diffuse, fine, reticular
pattern is observed. At times, the appearance is more nodular,
as reaction to the ova produces local densities in the interstitial tissue of the lung. The multiple
arteriovenous fistulae caused by the necrotizing arteritis result in
cyanosis with very little change noted on roentgenograms; this is a rare phenomenon. Occasionally, a
circumscribed nodule is produced by a granulomatous mass
surrounding an adult worm.21

NEMATHELMINTH
(ROUNDWORM) INFESTATION
Several roundworms cause pulmonary symptoms and transitory roentgen changes in the lungs as the larvae are carried to the
lungs through the veins or lymphatics.
As the larvae emerge from the alveolar capillaries into the bronchial tree, they produce an allergic response, usually
accompanied by eosinophilia. A combination of
edema and hemorrhage causes radiographic findings of patchy areas of poorly defined opacity scattered throughout the lungs.
The changes are transitory, and their
extent is related to the severity of the infestation. The following roundworms are among those causing such a reaction: Ascaris
lumbricoides, Strongyloides stercoralis,
Ancylostoma duodenale, and Necator americanus (hookworm). Ascariasis is often the cause of a Lffler's pneumonia, which
changes rapidly and usually clears in
about 10 days. Opportunistic pulmonary strongyloidiasis has been reported in compromised hosts, and it can be fatal. 49
However, it responds to treatment with
antihelminthic agents if recognized soon enough. The usual pulmonary reaction to Strongyloides is similar to the reaction to
Ascaris. In the opportunistic form, a
variety of lung manifestations have been described, including miliary, lobular, and lobar patterns. Cavitation or pleural effusion is
rare.
Filariasis caused by infestation with Filaria or Wuchereria bancrofti, Wuchereria malayi, or Loa loa is probably the cause of
tropical eosinophilia (see next section).
Dirofilaria immitis (dog heartworm) may also cause pulmonary disease in humans.75,76 Typically, it produces a solitary
pulmonary nodule, often peripheral, without
calcification and with a slightly irregular appearance. At first the small area of consolidation may be poorly defined; it then tends
to decrease in size over a few weeks
or months, after which it becomes more clearly defined. Rarely, multiple nodules are observed that may resemble pulmonary
metastases. They produce no symptoms.
Histologic examination of tissue is required to differentiate the nodule from tumor. Trichinella spiralis larvae usually produce no
pulmonary reaction as they pass
through the pulmonary circulation. In roundworm infestation, the diagnosis is made by discovery of the larvae or mature worm in
a stool specimen.

TROPICAL EOSINOPHILIA
Tropical eosinophilia or pulmonary eosinophilosis is manifested by symptoms of cough, fever,
lassitude, wheezing, chest pain, and sometimes dyspnea and weight
loss associated with an elevation of the leukocyte count. Eosinophilia is extreme (usually more than
3,000 eosinophils per cubic millimeter of blood) and persists for
weeks. Most reported cases originated in India, Indonesia, Sri Lanka, Pakistan, Southeast Asia, North
Africa, and some areas of South America. A few cases have
been reported in the United States and elsewhere throughout the world, primarily in persons who
had traveled to an endemic area. Some cases have been reported in
persons who had lived in India but had been away more than a year before the onset of symptoms.
The disease is mild and self-limited, but relapses may occur. Most
cases are definitely caused by filarial infestation, usually by W. bancrofti, and the disease usually
responds well to diethylcarbamazine, a drug effective in filariasis. 97
In other cases, the cause cannot be established.
Roentgen findings are of several types. The most common appearance is that of increased
pulmonary markings extending out from the hila, associated with mottled
parenchymal disease that is rather general in distribution. The hilar nodes may be enlarged. Next in
frequency is the addition of areas of patchy pneumonitis to the
small mottled densities. Increased markings alone are almost as common, and extensive scattered
involvement by a pneumonia-like process is noted occasionally.
The apices are usually spared. CT findings may resemble those of miliary TB or hypersensitivity
pneumonitis. On HRCT, small, centrilobular, rounded, nodular
opacities may be seen through the lung fields ( Fig. 24-68).

Tropical eosinophilia in
a 22-year-old man from
India with fever. Highresolution computed
tomography
demonstrates poorly
defined centrilobular,
nodular opacities
resulting from infection
by the filarial organism
Wuchereria bancrofti,
which causes a type of
hypersensitivity
reaction in the lung.
Findings mimic those of
miliary tuberculosis.