Imaging of Pulmonary Viral Pneumonia: Online CME

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Imaging of Pulmonary Viral

Pneumonia1
REVIEWS AND COMMENTARY
Tomás Franquet, MD, PhD

Imaging and clinical manifestations of viral pneumonia are
protean and not reliably predictive of its origin. All pa-
tients with neutropenic fever and normal findings at chest
radiography should undergo thin-section computed tomogra-
phy to determine whether parenchyma abnormalities are
present. Although the radiologic manifestations of viral
pneumonia are nonspecific and difficult to differentiate
from those of other infections, it is important to consider
viral infection when confronted with a rapidly progressive
pneumonia in patients with risk factors for infection. Al-
though definitive diagnosis cannot be made on the basis of
imaging features alone, the use of a combination of clini-
cal and radiographic findings can substantially improve
the accuracy of diagnosis in this disease.
Online CME
See www.rsna.org/ry_cme.html q
RSNA, 2011
Learning Objectives: Supplemental material: http://radiology.rsna.org/lookup

After reading the article and taking the test, the reader will /suppl/doi:10.1148/radiol.11092149/-/DC1
be able to
n Describe the role of thin-section thoracic CT in the
diagnosis viral pneumonia.
n Identify the most common features of pulmonary viral
infections at thin-section CT.
n Describe the most common viral infections in immuno-
competent and in immunocompromised patients.
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for Continuing Medical Education (ACCME) to provide
continuing medical education for physicians. The RSNA
designates this journal-based CME activity for a maximum
of 1.0 AMA PRA Category 1 Credit TM. Physicians should
only claim credit commensurate with the extent of their
participation in the activity.
Disclosure Statement
The ACCME requires that the RSNA, as an accredited
provider of CME, obtain signed disclosure statements
from authors, editors, and reviewers for this case. For
this journal-based CME activity, author disclosures
are listed at the end of this article. The editor and
the reviewers indicated that they have no relevant
relationships to disclose.
1
From the Department of Radiology, Hospital de Sant Pau,
Avda Sant Antoni M. Claret 167, Barcelona 08128, Spain.
Received November 19, 2009; revision requested January 7,
2010; revision received February 4; accepted February 17;
final version accepted March 1; final review by T.F.
February 24, 2011. Address correspondence to the
author (e-mail: tfranquet@santpau.cat ).
q
RSNA, 2011
18 radiology.rsna.org n Radiology: Volume 260: Number 1—July 2011

STATE OF THE ART: Imaging of Pulmonary Viral Pneumonia Franquet
M
ore than 55 million people die each up to 50%–64% of patients admitted to tive reaction that may be seen in a variety
year worldwide, and pneumonia the hospital with pneumonia. The recent of clinical contexts. In other words, orga-
is among the leading causes (1). development of multidetector helical com- nizing pneumonia may result from a vari-
Viral infections are an increasingly fre- puted tomographic (CT) scanners capa- ety of causes or underlying pathologic
quent cause of pulmonary disease world- ble of rapid scanning and acquisition processes, including viral infections.
wide. Unfortunately, the diagnosis of of thin sections has revolutionized the Most respiratory viruses damage cells
viral pneumonia still relies heavily on thin-section CT technique. Volumetric directly through cytopathic effects me-
clinician suspicion in the proper set- thin-section CT with thin detectors (0.5– diated by means of either viral-directed
ting, which is based on host risk fac- 0.625 mm) has become the routine in cell lysis or the inhibition of host cell
tors, presentation, and exposures. The many institutions. New serologic tests RNA, protein, and DNA synthesis. Other
diagnostic approach involves a consid- have also come to the aid of the clinician, viruses (eg, cytomegalovirus [CMV], ade-
eration of the likely pathogens on the and sophisticated molecular methods are novirus, or herpesvirus) may produce
basis of the patient’s presenting signs becoming more commonplace in routine specific nuclear changes or characteris-
and symptoms and his or her immuno- diagnosis of acute respiratory disease tic cytoplasmic inclusions (11) (Fig 1).
logic condition (2,3). The clinical mani- in both immunocompetent and high-risk Cytopathic respiratory viruses (eg,
festations of most viral infections are patients (1,6–8). Confirmation of the di- influenza, adenovirus, and herpesvirus
similar. Although most of these infec- agnosis and identification of the specific group) cause a virus-specific lung injury
tions in nonimmunocompromised per- agent can be accomplished with use of pattern. Influenza virus affects the epi-
sons are self-limited, some patients can tissue cultures, serologic tests, detection thelium diffusely and, in severe cases, re-
develop severe pneumonitis (4). Clini- of viral antigens within respiratory tract sults in necrotizing bronchitis and/or bron-
cally, viral pneumonia in adults can be secretions or blood with use of mono- chiolitis and diffuse alveolar damage.
divided into two groups: so-called atyp- clonal antibodies, detection of virus- The histologic features of influenza
ical pneumonia in otherwise healthy hosts associated molecules with use of in situ pneumonia are epithelial necrosis of the
and viral pneumonia in immunocom- hybridization or polymerase chain reac- airways with submucosal chronic inflam-
promised hosts (5). Influenza virus types tion (PCR), and observation of virus- mation. Fatal influenza pneumonia rep-
A and B account for most viral pneumo- induced changes cytologically or histolog- resents a necrotizing bronchiolitis with
nias in immunocompetent adults (5). It ically (9,10). The purpose of this review diffuse alveolar damage, which can be
has been considered that clinical his- is to provide a framework with which to hemorrhagic.
tory, results of physical examination, better understand respiratory viral infec- Adenovirus has its greatest effect in
and imaging features cannot enable the tions, the diverse clinical settings in which the terminal bronchioles and may pro-
prediction of the etiologic agent. Further- they occur, and their potential importance duce bronchiolitis or even bronchiectasis
more, a pathogen is identified in only in these varying clinical contexts. While (12–14). The bronchiolitis may be necro-
acknowledging the less-than-definitive tizing and result in a necrotizing broncho-
Essentials diagnostic role of CT in their diagnosis, pneumonia similar to that seen in severe
n Viral pulmonary infections are I will also include discussion of those herpes simplex infection (13) (Fig 2).
clinically important in both immu- conditions in which an understanding of The herpes group of viruses (herpes
nocompromised and immunocom- the pathologic characteristics can be use- simplex, varicella-zoster, CMV, Epstein-
petent patients; despite its limita- ful to the interpretation of thin-section Barr virus [EBV]) may cause focal cyto-
tions, CT is currently the imaging CT findings. The epidemiology and path- pathic effects in either the airway or
modality of choice for the evalua- ogenesis of viral infections are discussed alveoli. The histologic features of herpes
tion of pulmonary viral infections. in Appendix E1 (online). simplex lower respiratory tract infection
n Although the CT features of viral
pulmonary infections are usually Histologic Features of Viral Infections Published online
nonspecific, precise imaging char- 10.1148/radiol.11092149 Content codes:
Various histopathologic patterns of
acterization is essential; knowl-
lung injury have been described in viral Radiology 2011; 260:18–39
edge of CT findings has a substan-
pneumonia. Although some of these
tial effect on the treatment of Abbreviations:
patterns may be relatively unique to a AIDS = acquired immunodeficiency syndrome
patients suspected of having pul-
specific clinical context, others are non- CMV = cytomegalovirus
monary viral infections.
specific with respect to either the cause EBV = Epstein-Barr virus
n Knowledge of the underlying or pathogenesis. HMPV = human metapneumovirus
pathologic characteristics of Viruses can result in several patho- HTLV-1 = human T-cell lymphotropic virus type 1
these diseases aids in the differ- PCR = polymerase chain reaction
logic forms of lower respiratory tract
RSV = respiratory syncytial virus
entiation of viral infections from infection, including tracheobronchitis, SARS = severe acute respiratory syndrome
other entities that may have bronchiolitis, and pneumonia. Organiz-
overlapping imaging features. ing pneumonia is a nonspecific repara- Author stated no financial relationship to disclose.
Radiology: Volume 260: Number 1—July 2011 n radiology.rsna.org 19

Figure 1 Figure 2 Figure 3
Figure 2: Histopathologic features of respiratory

Figure 1: Histopathologic features of pulmo- syncytial virus (RSV) bronchiolitis in a child. Photo-
Figure 3: Histopathologic features of necrotizing
nary CMV infection. Photomicrograph (hematoxylin- micrograph (hematoxylin-eosin stain; original mag-
herpes pneumonia. Image from scanning low-power
eosin stain; original magnification, 3400) nification, 3400) shows two adjacent bronchioles
microscopy (hematoxylin-eosin stain; original mag-
shows numerous CMV-infected cells; they are with a marked transmural cellular infiltrate (bronchi-
nification, 320) shows nodular zones of necrosis,
enlarged and contain nuclei with prominent olitis) (arrowheads) and some associated meta-
some of which are bronchiolocentric (arrows).
amphophilic inclusions (arrowheads). (Image plastic changes in the mucosa. Ulcerative mucosal
(Image courtesy of T. Colby, MD, Mayo Clinic,
courtesy of T. Colby, MD, Mayo Clinic, Scotts- changes are also seen (arrow). (Image courtesy of T.
Scottsdale, Ariz.)
dale, Ariz.) Colby, MD, Mayo Clinic, Scottsdale, Ariz.)
include necrosis of the airway epithelium, Coxsackievirus B, reoviruses, and damage (intraalveolar edema, fibrin,
necrotizing pneumonia as the reaction rhinoviruses may also infect the lungs, and variable cellular infiltrates with a
spreads from the airways to the adjacent usually producing interstitial pneumonias hyaline membrane), intraalveolar hem-
parenchyma, diffuse alveolar damage, with diffuse alveolar damage. Human orrhage, and interstitial (intrapulmonary
miliary nodules, and scattered larger nod- papilloma viruses are known to cause re- or airway) inflammatory cell infiltra-
ules (15) (Fig 3). Multicentric areas of current papillomas and have been linked tion (20).
hemorrhage may appear centered on air- to lung cancer.
ways. An acute lung injury pattern may In immunocompetent individuals,
be present, with interstitial edema, con- RSV and parainfluenza viruses may pro- Clinical Manifestations
gestion, and inflammation. Histologic duce necrotizing bronchiolitis charac- The clinical signs and symptoms of viral
features of varicella-zoster virus pneu- terized by exudates within bronchiolar pneumonia are often nonspecific, and
monia include endothelial damage in small lumen, inflammatory cells in the wall the clinical course of infection will be
vessels, with focal hemorrhagic necro- of bronchioles, a peribronchiolar reac- highly dependent on the overall immune
sis, mononuclear infiltration of alveolar tion with chronic inflammatory cells, and status of the host (3). Acute bronchioli-
walls, and fibrinous exudates in the alve- exudate in alveoli. In immunocompro- tis is a term most often used to describe
oli (16). Late sequelae of varicella-zoster mised patients, parainfluenza viruses an illness in infants and children char-
infection consist of multiple 1–2-mm- produce giant cell pneumonia with dif- acterized by acute wheezing with con-
diameter calcified nodules (17). fuse alveolar damage indistinguishable comitant signs of respiratory viral infec-
The histologic findings in CMV pneu- from that caused by measles pneumonia. tion (21). RSV is the etiologic agent in most
monia include either an acute intersti- Measles virus may involve both air- patients, but other viruses (adenovirus,
tial pneumonia or a miliary pattern. Acute ways and lung parenchyma, producing influenza, parainfluenza) and nonviral
interstitial pneumonia is characterized bronchitis and/or bronchiolitis and in- pathogens (mycoplasma, Chlamydia spe-
by a diffuse mild alveolar widening by terstitial pneumonia. cies) can cause a similar syndrome (22).
edema and mononuclear cells, airspace The predominant pathologic process Symptomatic acute bronchiolitis in
fibrinous exudate and/or hyaline mem- of hantavirus pulmonary syndrome and adults is relatively rare but can be caused
branes with relatively scant neutrophils, severe acute respiratory syndrome (SARS) by infectious agents such as RSV. Be-
and prominent type 2 alveolar lining cells is diffuse alveolar damage and diffuse cause small airways in adults contribute
(Fig 4); foci of organizing pneumonia lung disease characterized histologically less to total pulmonary resistance, acute
are often found. The miliary pattern is by interstitial edema and central alveo- infectious bronchiolitis may spare adults
similar to that of other miliary viral in- lar filling (18,19) (Fig 5). the severe symptoms characteristic of
fections; nodules contain the infected The radiologic findings reflect the bronchiolitis in infants. Acute bronchi-
cells with the characteristic cytoplasmic variable extent of the histopathologic olitis in adults may also be seen with
inclusions of CMV. features, which include diffuse alveolar aspiration, toxic inhalation, connective

Figure 4 Figure 5 and not invariably associated with pneu-

monia; lower respiratory tract symp-
toms are found in 10% of cases (3).
Laboratory Identification Methods

Differentiation of common respiratory
infections due to Streptococcus pneu-
moniae and those due to Mycoplasma
pneumoniae, Chlamydophila pneumo-
niae, or Legionella pneumophila as well
as those due to viruses is essential to
allow correct decisions concerning the
antibiotics to be administered (3).
Figure 4: Histopathologic features of a CMV inter- Figure 5: Histopathologic features of diffuse Diagnosis of respiratory viruses is
stitial pneumonia. Photomicrograph (hematoxylin- alveolar damage in a patient with SARS. Photomi- still difficult, with only a small percent-
eosin stain; original magnification, 3100) shows crograph (hematoxylin-eosin stain; original magnifi- age of cases being routinely diagnosed.
interstitial widening with formation of micronodules cation, 3200) demonstrates that alveolar septa Although viral culture has been the ref-
(arrows). This is associated with acute lung injury show complete loss of epithelium and are lined by erence standard, it has considerable lim-
and some hyaline membranes (arrowheads). (Image hyaline membranes (arrowheads); intraalveolar itations (ie, depending on the virus, it
courtesy of T. Colby, MD, Mayo Clinic, Scottsdale, edematous material is also present (arrows). (Image
may take 3–14 days for cultures to yield
Ariz.) courtesy of T. Colby, MD, Mayo Clinic, Scottsdale,
results).
Ariz.)
The development of better diagnos-
tissue diseases, lung and bone marrow tic tests has markedly improved our
transplantation, and Stevens-Johnson cause can be established with certainty ability to detect multiple viral patho-
syndrome (23). only in approximately 50% of patients gens (3). These techniques include cul-
Pathologic studies of acute infec- with pneumonia. The probable predom- ture to prove replication of complete
tious bronchiolitis have shown intense inant organism varies with the host’s epi- viral particles, hybridization techniques
acute and chronic inflammation of small demiologic factors, the severity of illness, performed with or without PCR to de-
bronchioles with associated epithelial and the laboratory approach used to es- tect viral nucleic acids, immunohisto-
necrosis and sloughing. There may be tablish the diagnosis. chemistry to detect viral proteins, elec-
associated edema as well as inflamma- Although most attention traditionally tron microscopy to demonstrate a fully
tory exudate and mucus in the bron- focuses on bacterial causes of severe assembled virus, and measurements of
chiolar lumen (24). community-acquired pneumonia, viruses a specific host immune response to the
The possibility of pneumonia should can also cause serious lower respiratory virus in either serum or cells or tissue.
be considered in any patient who has new tract infections. The predominant re- The most appropriate specimens are
respiratory symptoms (including cough, spiratory viruses that can cause severe nasopharyngeal aspirates, nasopharyn-
sputum, or dyspnea), particularly when pneumonia include influenza and RSV. geal and throat swabs, and those from
these symptoms are accompanied by fever The clinical manifestations of viral bronchoalveolar lavage (26).
or abnormalities at physical examination infections often vary from patient to pa-
of the chest (eg, rhonchi and rales). tient and cannot be reliably used to es- Nucleic Acid Amplification Tests
Pneumonia is also increasingly prev- tablish a specific (microbiologic) diagno- The introduction of highly sensitive nu-
alent in patients with specific comorbidi- sis. The initial symptoms and signs may cleic acid amplification tests has dra-
ties or risk factors, including smoking, be categorized into several clinical syn- matically improved the ability to detect
chronic obstructive pulmonary disease, dromes (25). A “cold” is characterized multiple respiratory viruses such as in-
asthma, diabetes mellitus, malignancy, by upper respiratory tract symptoms fluenza, RSV, rhinovirus, parainfluenza,
heart failure, neurologic diseases, nar- and includes tonsillopharyngitis, phar- and adenovirus (27–29).
cotic and alcohol use, and chronic liver yngitis, epiglottitis, sinusitis, otitis me- The most familiar formats use DNA
disease. dia, and conjunctivitis. The “influenza” or RNA target amplification methods for
A thorough physical examination, pos- syndrome, which may be caused by viruses enhanced sensitivity above that of culture
teroanterior and lateral chest radiog- other than influenza, consists primar- and antigen-based procedures (28).
raphy, and a blood leukocyte count with ily of abrupt fever, headache, myalgias,
a differential cell count should be per- and malaise. The disease manifestations PCR
formed when pneumonia is suspected. of several viruses (eg, human parainflu- The value of PCR in identifying respi-
Even with intensive laboratory in- enza virus, RSV, and influenza) are often ratory viruses in clinical samples has
vestigation, the specific microbiologic confined to the upper respiratory tract been clearly shown, and as much as a

three- to fourfold increase in positive spec- associated with increased frequency and attenuation pattern) are a recognized
imens has been found when PCR test- severity of viral infections include very finding in some viral infections caused
ing is added to conventional cell culture young and old age, malnutrition, and by hypoventilation of alveoli distal to
and/or “standard” serologic methods. The immunologic disorders. bronchiolar obstruction (inflammation or
downside of PCR is that it may be too sen- Chest radiographs demonstrate nor- cicatricial scarring of many bronchioles),
sitive, in that it can detect small amounts mal findings or unilateral or patchy bi- which leads to secondary vasoconstric-
of residual viral nucleic acid when there lateral areas of consolidation, nodular tion (and, consequently, underperfused
is no other laboratory or clinical evidence opacities, bronchial wall thickening, and lung) and is seen on CT scans as areas
that a viral infection is present. Factors small pleural effusions; lobar consolida- of decreased attenuation (44–46). Paired
that lead to negative laboratory results tion is uncommon in patients with viral CT scans obtained in inspiration and
include poor specimen handling and col- pneumonia. Patients may develop acute expiration are useful for differentiating
lection, low viral copy numbers, and in- pneumonia with rapid progression to bronchiolar disease from pulmonary vas-
hibitors in the clinical sample (10). acute respiratory distress syndrome. cular disease and some diffuse infiltrative
Although radiographic findings alone diseases that may also cause a mosaic
Reverse Transcriptase PCR are not sufficient for the definitive diagno- pattern. In bronchiolar disease, the re-
Reverse transcriptase PCR is a modi- sis of viral pneumonia, in combination gions of decreased attenuation seen in
fication of PCR used when the initial with clinical findings they can substan- the lung at inspiration are also seen at
template is RNA rather than DNA. Reverse tially improve the accuracy of diagnosis expiration owing to air trapping and show
transcriptase PCR can be used to am- in this disease. little increase in attenuation or decrease
plify a much higher number of DNA copin volume as seen with primary vascular
ies present in bacteria, fungi, virus, or Thin-Section CT Findings lung disease (47,48) (Fig 6).
other proteins (10). An increasing number of patients un- Uninvolved segments of lung show
Despite the obvious advantages of dergo thin-section CT when there is high normal or increased perfusion with re-
these newer procedures, there may be clinical suspicion of pneumonia with nor- sulting normal or increased attenuation,
potential limitations to DNA amplifica- mal or questionable radiographic find- respectively. In the specific context, co-
tion technology in the diagnostic micro- ings (32–38). In a study of 87 consec- existing inflammatory small airways and
biology laboratory, as follows: (a) False- utive patients with febrile neutropenia, parenchyma disease may both contribute
negative test results may occur because Heussel et al (39) noted that the CT scan to a mosaic attenuation pattern (49).
of the presence of substances in the revealed a pulmonary lesion not seen Nevertheless, differentiation between
specimen that inhibit nucleic acid extrac- on the radiograph in 50% of subjects. the various causes of a mosaic attenuation
tion or amplification, (b) careful inter- The CT signs of pulmonary viral in- pattern on CT scans (diffuse infiltrative,
pretation of results is necessary, (c) the fection will depend on the underlying small airways, and occlusive vascular dis-
procedure is technically complex, (d) pathologic process. They are quite sim- eases) is not always straightforward and
equipment is expensive, and (e) there is ilar simply because the underlying path- may, on occasion, cause diagnostic dif-
a lack of standardization (30,31). ogenic mechanism, depending on the ficulties (45,48).
virulence of the virus, is related to var- Ground-glass opacity and consoli-
iable extents of histopathologic features dation.—A ground-glass opacity is a hazy
Imaging of Viral Pneumonia such as diffuse alveolar damage (intraal- increase in attenuation seen in a variety
In patients suspected of having viral pneu- veolar edema, fibrin, and variable cellu- of interstitial and alveolar processes. In
monia, imaging is performed to help de- lar infiltrates with a hyaline membrane), the context of pulmonary infectious
tect disease, assess disease extent, per- intraalveolar hemorrhage, and intersti- diseases, coexisting thickening of the
form follow-up assessment of response tial (intrapulmonary or airway) inflam- interstitium and partial filling of the air-
to treatment, and guide interventional matory cell infiltration (40,41). spaces may both contribute to ground-
diagnostic procedures (eg, bronchos- The spectrum of CT findings encoun- glass opacity and consolidation (Fig 7).
copy with bronchoalveolar lavage). tered in various pulmonary viral diseases Nevertheless, other noninfectious con-
It can be difficult to differentiate viral is not particularly wide and encompasses ditions characterized by ground-glass
pneumonia from other infectious pro- five main categories: (a) parenchymal opacity include interstitial pulmonary
cesses, and the cause of infection (eg, attenuation disturbances; (b) ground- edema, pulmonary hemorrhage (in which
viral vs pyogenic or fungal) cannot be glass opacity and consolidation; (c) nod- there is thickening of the interstitium
reliably ascertained from its imaging ules, micronodules, and tree-in-bud opac- and partial filling of the airspaces with
appearance. ities; (d) interlobular septal thickening; blood), hypersensitivity pneumonitis, re-
and (e) bronchial and/or bronchiolar spiratory bronchiolitis, organizing pneu-
Conventional Radiographic Findings wall thickening (42,43). monia, and alveolar proteinosis (50–54).
Radiologic features are dependent on Parenchymal attenuation distur- Areas of pulmonary consolidation are
several host factors, including age and bances.—Patchy inhomogeneities in the most often patchy and poorly defined
underlying immune status; risk factors attenuation of lung parenchyma (mosaic (consistent with bronchopneumonia) or

Figure 6 Figure 7
Figure 6: Transverse expiratory thin-section CT scan through the

lower lobes in a 44-year-old woman with constrictive obliterative bron-
chiolitis secondary to a severe viral lower respiratory tract infection.
There are bilateral well-demarcated patchy areas of increased and
Figure 7: Transverse thin-section CT scan at the level of the bron-
decreased lung attenuation. Whereas hypoattenuated areas contain few
chus intermedius in a patient with RSV infection shows a hazy increase
and small pulmonary vessels (arrows), hyperattenuated areas contain
in lung opacity without obscuration of underlying vessels.
enlarged pulmonary vessels (arrowheads), reflecting the pulmonary
blood flow distribution toward normal ventilated areas.
Figure 9
Figure 8
Figure 9: Transverse thin-section CT scan through the lower lobes in a

Figure 8: Transverse thin-section CT scan at the level of the bron- patient with influenza A virus infection shows bilateral multiple small
chus intermedius in a patient with influenza A virus shows ill-defined branching opacities (arrows) representing dilated peripheral bronchioles.
centrilobular nodules (arrows). Peripheral subpleural consolidation
in the apical segment of left lower lobe (arrowhead) represents Centrilobular nodules are most com-
coalescence of nodules. monly seen in patients with disease that
primarily affects centrilobular bronchioles
focal and well-defined (consistent with ameter may be seen in a number of lung and results in inflammation, infiltration,
lobar pneumonia). As with consolida- infections. Nodule size is helpful in the or fibrosis of the surrounding interstitium
tion, a variety of acute and chronic lung differential diagnosis of infectious causes and alveoli (55) (Fig 8). These nodules
diseases may result in lobular areas of of nodules. Franquet et al (37) compared may be dense and of homogeneous atten-
ground-glass opacity, which give the lung the CT findings in 78 consecutive immu- uation or show ground-glass opacity.
a mosaic appearance. Lobular ground- nocompromised patients with solitary or The tree-in-bud finding, which is usu-
glass opacity may be seen in patients multiple nodular opacities of proved in- ally indicative of small airways disease,
with infection (eg, bronchopneumonia, fectious origin. There was a good cor- reflects the presence of dilated centri-
viral infections, Pneumocystis jirovecii relation between the size of the nodules lobular bronchioles with lumina that
pneumonia, or M pneumoniae). and their origin. Patients whose nodules are impacted with mucus, fluid, or pus;
Nodules, micronodules, and tree-in- were smaller than 10 mm in diameter this finding is often associated with
bud opacities.—Nodules 1–10 mm in di- were most likely to have a viral infection. peribronchiolar inflammation (56) (Fig 9).

Figure 10 Figure 11
Figure 10: Transverse thin-section CT scan through the lower lobes

in a patient with adenovirus infection shows patchy bilateral ground- Figure 11: Transverse thin-section CT scan at the level of the aortic
glass opacities with superimposed linear opacities (crazy-paving arch in a patient with parainfluenza virus infection shows bilateral
pattern) (arrows). ground-glass opacities and bronchial wall thickening (arrows).
Furthermore, in most cases, a tree-in- chioles by inflammatory exudates and try of the virus capsid (helical vs icosa-
bud appearance is associated with air- bronchiolar wall thickening from edema hedral), and (c) the presence or absence
ways infection. Infectious diseases asso- and smooth muscle hyperplasia proof a lipid envelope.
ciated with cellular bronchiolitis and duce the thin-section CT features of The respiratory viruses can be di-
centrilobular nodules include endobron- atelectasis, air trapping, centrilobular vided into two large groups according
chial spread of tuberculosis, nontuber- nodules, and bronchiolar wall thickening. to the type of nuclei acid they contain
culous mycobacteria bronchopneumo- Air trapping may be present because of (Table 2).
nia (57–62), and infectious bronchiolitis associated bronchiolitis (Fig 11). A sum-
(56). Branching or centrilobular nodules mary of CT findings in viral pneumonia Selected RNA Virus–related Diseases
and mosaic perfusion are seen in pa- is shown in Table 1. Influenza.—Influenza viruses are single-
tients with viral bronchiolitis (63,64). In clinical practice, radiologists will stranded RNA viruses that belong to
Similar findings may also be observed have to consider that there are many the family Orthomyxoviridae. Influenza
with bacterial and fungal pneumonia noninfectious or different infectious dis- viruses are important human respira-
and in patients with allergic bronchopul- orders that should be differentiated from tory pathogens that cause seasonal upper
monary aspergillosis (65). viral pneumonia. A combined strategy respiratory tract infections in the com-
Interlobular septal thickening.—Sep- consisting of thin-section CT and guided munity, endemic infections, and periodic,
tal thickening may be seen in the pres- bronchoscopy with bronchoalveolar la- unpredictable pandemics (70). The great-
ence of interstitial fluid, cellular infiltra- vage performed within the first 24 hours est influenza pandemic, the so-called
tion, or fibrosis and can have a smooth, after CT could improve the diagnos- Spanish influenza, spread worldwide in
nodular, or irregular contour in different tic yield and subsequent therapeutic 1918 and resulted in the deaths of ap-
pathologic processes. In the context of changes in these patients. proximately 50 million people (71,63).
viral diseases, the most dramatic cause Influenza type A is the most impor-
of widespread smooth thickening of the tant of the respiratory viruses with re-
interlobular septa is acute respiratory Viral Pathogens of the Respiratory spect to the morbidity and mortality in
distress syndrome (66). Tract the general population. They are more
Smooth septal thickening may also Viral infections of the respiratory tract common during infancy and often may
be seen in association with ground-glass include both those considered to be prin- lead to severe lower respiratory tract
opacity, a pattern termed “crazy pav- cipal respiratory viruses, whose replica- disease. In adults, infections are usually
ing” (Fig 10); this pattern, initially de- tion is generally restricted to the respi- mild and restricted to the upper respi-
scribed as typical of alveolar proteinosis, ratory tract, and others whose respira- ratory tract. Influenza A virus is trans-
has an extensive differential diagnosis tory involvement is part of a generalized mitted from person to person by aero-
(27,67–69). infection. Viruses are classified on the solized or respiratory droplets. In the
Bronchial and bronchiolar wall thick- basis of (a) the type and structure of United States, more than 35 000 deaths
ening.—Bronchiolar wall thickening may the nucleic acid in the viral genome and and 200 000 hospitalizations due to in-
occur due to inflammation or fibrosis. the strategy used in its replication (eg, fluenza occur annually, and the number
In viral bronchitis, obstruction of bron- DNA or RNA), (b) the type of symme- is increasing (64).

Table 1
Summary of CT Findings in Viral Pneumonia
Parenchymal Ground-Glass Nodules, Micronodules, Interlobular Bronchial and/or
Attenuation Opacity and and Tree-in-Bud Septal Bronchiolar Wall
Cause of Pneumonia Disturbances Consolidation Opacities Thickening Thickening Other
RNA viruses
Influenza A … +++ +++ … … …
Avian flu (H5N1) … +++ + … … Pneumatocele, pleural effusion
Swine-origin influenza A (H1N1) … +++ … … … …
Parainfluenza 1–4 … +++ +++ … … …
RSV … +++ +++ … +++ …
HMPV* … +++ +++ … … …
Measles … +++ +++ ++ ++ Pleural effusion, lymphadenopathy
Enteroviruses … … … … … …
Hantavirus … +++ ++ +++ … Acute respiratory distress syndrome
Coronavirus (SARS) … +++ … +++ … Crazy-paving pattern
DNA viruses
Adenovirus … ++ … … +++ Bronchiectasis
Herpes simplex virus … +++ ++ … … Nodules with halo sign
Varicella … ++ +++ … … Nodules with halo sign or calcified
CMV … +++ ++ … … Nodules with halo sign
EPV … +++ + + … Nodules with halo sign
Note.—Plus signs indicate the relative frequency of the findings from lowest (+) to highest (+++).
* HMPV = human metapneumovirus.
Table 2 Avian flu (H5N1).—Avian influenza

is caused by the H5N1 subtype of the
Selected Viruses Causing Respiratory Syndromes influenza A virus (73,74). Most human
Family Species and Subtype infections appear to be the result of
close contact with infected birds—usually
RNA viruses
poultry or their products (73,75,76).
Orthomyxoviridae Influenza A (subtype: avian flu [H5N1], swine-origin
In May 1997, an influenza H5N1 virus
influenza A [H1N1]), influenza B
was isolated from a previously healthy
Paramyxoviridae Parainfluenza 1–4, measles
3-year-old boy in Hong Kong who died
Metapneumoviridae RSV, HMPV
Picornaviridae Enteroviruses
of severe pneumonia complicated by acute
Retroviruses HTLV-1* respiratory distress syndrome (77). In
Bunyaviridae Hantavirus November and December of the same
Coronaviridae Coronaviruses (subtype: SARS coronavirus) year, 18 additional cases of human H5N1
DNA virus (Adenoviridae) Adenovirus, herpes simplex virus (HSV), varicella-zoster infections were identified—six of which
virus, CMV, EBV, human papilloma virus were fatal (78). According to World Health
Organization statistics, as of June 19,
* HTLV-1 = Human T-cell lymphotropic virus type 1.
2008, 385 human infections had been
confirmed from 15 countries; of these
infections, 243 were fatal. Approximately
The symptoms of influenza begin including solid organ transplant recip- 90% of confirmed infections have been
rapidly with fever, usually 101°–102°F ients (72). Oikonomou et al (65) re- in persons 40 years of age and younger.
(38°–39°C), and is associated with myal- viewed the thin-section CT findings in Most of those infected were previously
gias, headache, lethargy, and respira- four patients with hematologic malig- healthy individuals. Signs and symp-
tory tract symptoms of dry cough, rhin- nancies and influenza A pneumonitis toms of infection included fever, cough,
orrhea, and sore throat. and found that the predominant thin- diarrhea, shortness of breath, lympho-
In recent years, both influenza and section CT findings were ground-glass cytopenia, and thrombocytopenia. The
parainfluenza viruses have been rec- opacities, consolidation, centrilobular overall case fatality rate for influ-
ognized as a major cause of respiratory nodules, and branching linear opacities enza A (H5N1) infections exceeds 60%
illness in immunocompromised patients, (Fig 12). (79–81).

Figure 12 Figure 13
Figure 12: Transverse thin-section CT scan through the upper lobes

in a patient with influenza pneumonia shows extensive bilateral ground-
glass opacities. Areas of ground-glass opacity are associated with
both intra- and interlobular septal thickening (crazy-paving pattern). Figure 13: Transverse thin-section CT scan at the level of the bron-
chus intermedius in a patient with avian flu H5N1 pneumonia shows
Most chest radiographs are abnormal a rounded area of consolidation (arrow) surrounded by ground-
at presentation, with multifocal consol- glass opacity in the lingula.
idation the most common radiographic
finding. The most common CT findings monia in 18 patients with proved swine- of seasonal upper respiratory tract infec-
consist of focal, multifocal, or diffuse origin influenza A virus; 12 of the 18 tion in adults and children (92). Human
ground-glass opacities or areas of con- patients required mechanical ventilation parainfluenza virus is genetically and anti-
solidation (76) (Fig 13). Pseudocavita- and seven died. genically divided into types 1–4. Although
tion, pneumatocoele formation, lymph- On June 11, 2009, the World Health parainfluenza types 1–4 are all respiratory
adenopathy, and centrilobular nodules Organization declared the first pandemic pathogens in humans, types 1–3 are the
are often seen. During the course of of the 21st century caused by swine- most common cause of disease (93).
disease, pleural effusions and cavitation origin influenza virus A (H1N1) (87). Ac- Recently, parainfluenza virus type 3
can also develop (76). tually, the virus continues to spread glob- has been recognized as a substantial
Reverse transcriptase PCR is the ally and its transmission among humans cause of respiratory illness in immuno-
most commonly used test for diagnos- appears to be high; however, its viru- compromised patients, including solid
ing H5N1 infection (6). The test can be lence is not greater than that observed organ transplant recipients (94).
done on nasal and pharyngeal swabs, with seasonal influenza (85,87). The dis- The CT findings of parainfluenza virus
respiratory specimens, blood, cerebro- ease has spread rapidly since then, with infection are variable, consisting of multi-
spinal fluid, and feces (82). 254 206 cases having been documented ple small peribronchial nodules, ground-
Swine influenza (H1N1).—In the worldwide as of September 7, 2009, and glass opacities, and airspace consolida-
spring of 2009, an outbreak of severe an estimated 2837 deaths (88). tion (94–96) (Fig 15).
pneumonia was reported in conjunction Reverse transcriptase PCR is the most RSV.—RSV is a ubiquitous cause of
with the concurrent isolation of a novel commonly used test for making a clini- respiratory infection, with a worldwide
swine-origin influenza A (H1N1) virus, cal diagnosis of H1N1 infection and dif- distribution and seasonal occurrence.
widely known as swine flu, in Mexico ferentiating it from seasonal influenza RSV is the most frequent viral cause of
(approximately 1600 cases) (83). viruses (89,90). lower respiratory tract infection in in-
Although it seems that the virulence The predominant CT findings are fants (97). The major risk factors for
of this microorganism is not currently unilateral or bilateral ground-glass opac- severe RSV disease in children are pre-
very high, and in most of the infected ities with or without associated focal or maturity (,36 weeks gestation), congen-
patients it only causes a mild respira- multifocal areas of consolidation. At mul- ital heart disease, chronic lung disease,
tory disease, some deaths, particularly tidetector CT, the ground-glass opacities immunocompromised status, and mul-
in Mexico, have been reported (84,85). and areas of consolidation have a pre- tiple congenital abnormalities (21,68).
The cause of these deaths is not yet dominant peribronchovascular and sub- In immunocompetent adults, RSV in-
known but logically they could be due pleural distribution, resembling organiz- fection usually manifests with rhinor-
to severe pulmonary complications such ing pneumonia (91) (Fig 14). rhea, pharyngitis, cough, bronchitis, head-
as acute respiratory distress syndrome Parainfluenza virus.—Parainfluenza ache, fatigue, and fever. In older persons,
or secondary pneumonia. Perez-Padilla viruses belong to the family Paramyxoviri- particularly those with chronic cardio-
et al (86) reported bilateral patchy pneu- dae and are known to be a common cause pulmonary illnesses, severe pneumonia

Figure 14 Figure 15
Figure 14: Coronal reformation multidetector CT scan in a 46-year- Figure 15: Transverse thin-section CT scan through the lower lobes
old man with swine-origin influenza A (H1N1) viral infection shows bilat- in a patient with parainfluenza pneumonia shows a central area of
eral lobular and subsegmental areas of consolidation involving mainly consolidation in the right lower lobe and ground-glass opacities
the subpleural lung regions (arrowheads). in the left lower lobe.
may occur, leading to respiratory fail- illness occurs in premature infants with to the family Paramyxoviridae that causes
ure. It is a known cause of life-threaten- or without chronic lung disease and in- a febrile illness with rash in children.
ing pneumonia in hematopoietic stem cell fants and young children with congen- Measles virus is highly contagious and
transplant recipients and those with he- ital heart disease (100,101). transmitted from person to person by
matologic malignancies. In adults, epidemiologic studies have either aerosolized droplet nuclei or di-
Gasparetto et al (98) reviewed the demonstrated that HMPV infection ac- rect contact with contaminated respira-
thin-section CT findings in 20 patients counted for 4% of cases among patients tory secretions. After an incubation time
with RSV pneumonitis after hematopoi- with community-acquired pneumonia or of almost 2 weeks, disease starts with a
etic stem cell transplantation and found chronic obstructive pulmonary disease prodromal phase of fever, cough, and
that the predominant patterns of abnor- exacerbations (102,103) and caused a coryza (106). A few days later, a general-
mality were small centrilobular nodules nonspecific respiratory illness in more ized maculopapular skin rash appears—
(50%), airspace consolidation (35%), than 2% of patients with cancer (104). often in combination with conjunctivitis.
ground-glass opacities (30%), and bron- Moreover, HMPV accounted for 9% of Whereas mild pulmonary infection
chial wall thickening (30%) (Fig 16). all acute respiratory infections in pa- often occurs in healthy adults, severe
The abnormalities were located in the tients with hematologic malignancies, pneumonia, with an often protracted and
central and peripheral areas of the lungs with a mortality rate of 11% in the sub- fatal course, may occur in immunocom-
and manifested with a predominantly set of patients who developed lower re- promised and debilitated patients. The
bilateral and asymmetric distribution. spiratory infection (99). mortality in adult measles pneumonitis
HMPV.—HMPV is a recently identi- Recently, Franquet et al (105) re- appears to be lower than that in chil-
fied RNA virus, genus Metapneumovirus. viewed CT findings in five patients with dren; the reported mortality rates vary
Like RSV, HMPV is usually associated HMPV pneumonia and found that the considerably, from 1% up to 36% (107).
with acute respiratory tract infections predominant findings were patchy areas CT findings of measles pneumonia
including upper airway disease, lower of ground-glass attenuation, small nod- are nonspecific and include bronchial wall
airway bronchitis and bronchiolitis, in- ules, and multifocal areas of consolidation thickening, centrilobular nodules, ground-
fluenza-like syndrome, and pneumonia. in a bilateral asymmetric distribution glass opacity, interlobular septal thicken-
Although HMPV has been implicated (Fig 17). Pulmonary parenchymal in- ing, pleural effusion, and lymphadenop-
in 4%–21% of infants with acute bron- volvement during the course of HMPV athy (20,107–109) (Fig 18 ). Nakanishi
chiolitis, their symptoms are clinically pneumonia infection may result in in- et al (110) reported that centrilobular
indistinguishable from those elicited by terstitial lung disease and fibrosis. nodules, ground-glass opacity, and in-
RSV (99). Children typically present with Measles.—Measles is one of the three terlobular septal thickening may indi-
rhinorrhea, fever exceeding 100.4°F major infectious diseases worldwide and cate a measles-specific, virus-induced
(.38°C), nonproductive cough, pro- causes approximately 1.5 million child- pneumonia.
gressive dyspnea, hypoxemia, and bron- hood deaths per year. Measles is a single- In most measles cases, diagnosis is
chiolitis. An increased risk for severe stranded RNA enveloped virus belonging based on clinical symptoms only. The

Figure 16 Figure 18
Figure 16: Transverse thin-section CT scan through the upper lobes

in a patient with respiratory syncytial pneumonia shows bilateral Figure 18: Transverse thin-section CT scan at the level of the carina
ill-defined centrilobular nodules (arrows) and bronchial wall in a patient with measles infection shows multiple centrilobular nodules
thickening (arrowhead). (arrowhead) and bilateral areas of lobular consolidation (arrows).
Figure 17 count for most viruses recovered from and thickening of the bronchovascular
children with summertime upper respi- bundles in the peripheral lung (121).
ratory tract infections (112). Most infec- Hantavirus.—The genus Hantavirus
tions are not associated with pneumonia. comprises a genetically homogeneous
Lower respiratory tract infection may group of enveloped, single-stranded RNA
occur sporadically, and some enteroviruses belonging to the family Bunya-
virus serotypes are capable of producing viridae. During the spring of 1993, an
fulminant, frequently fatal disease in emerging rodent-borne zoonotic disease,
the newborn infant. In the first few characterized by severe acute respira-
days of life, fatal cases of enterovirus tory failure, rapid clinical progression,
pneumonia caused by echovirus types and high case-fatality rates, occurred
6, 9, and 11 and group A coxsackievirus among healthy adults in the southwest-
type 3 have been reported (113–115). ern United States (122).
Enterovirus 69 has been isolated from Hantavirus infection may cause dif-
the throat secretions of infants with bron- fuse airspace disease, termed hantavirus
Figure 17: Close-up view of transverse thin- chiolitis and pneumonia (116). pulmonary syndrome (123). The incu-
section CT scan at the level of the right lower lobe HTLV-1.—HTLV-1 is an RNA retro- bation period for hantavirus pulmonary
in a patient with HMPV infection after hematopoi- virus. It is the first retrovirus to be as- syndrome is typically 1–2 weeks but
etic stem cell transplantation shows multiple centri- sociated with human disease (117). It is ranges from 1 to 4 weeks. The prodromal
lobular nodules (arrows) and focal areas of transmitted by sexual contact, by blood stage is usually 3–5 days (range, 1–10
consolidation (arrowhead). transfusion, from mother to child trans- days) (124). Patients have an abrupt
placentally, and via breast feeding. onset of symptoms, which include fever,
The lung is a preferential site for myalgia, malaise, chills, anorexia, and
most common method is the demon- HTLV-1 infection (118). HTLV-1 is an headache.
stration of measles virus–specific IgM in a etiologic retrovirus of adult T-cell leuke- Although hantavirus pulmonary syn-
single serum sample, but a more than mia or lymphoma (117,119). Myelopa- drome and acute interstitial pneumonia
fourfold titer increase in paired serum thy, Sjögren syndrome, and lymphocytic can share similar clinical presentations,
samples is also formal proof of a recent pneumonitis have been reported in as- acute interstitial pneumonia and fatal
measles virus infection. Virus detection sociation with HTLV-1 infection (120). cases of hantavirus pulmonary syndrome
may be performed by means of virus iso- Clinical-pathologic and radiologic can generally be differentiated on clini-
lation or reverse transcriptase PCR (111). similarities have been demonstrated in cal and histologic grounds, and this dis-
Coxsackievirus, echovirus, and entero- patients with HTLV-1–associated bron- tinction can be further confirmed immu-
virus.—Coxsackievirus is a RNA virus, chiolitis and in those with diffuse pan- nohistochemically (18).
genus Enterovirus. The human neonate bronchiolitis (121). CT findings in pa- Histologically, changes are charac-
is uniquely susceptible to coxsackievirus tients with HTLV-1 consist mainly of cen- teristic for exudative (eg, focal hya-
and echovirus disease. Enteroviruses ac- trilobular nodules, ground-glass opacity, line membranes, extensive intraalveolar

Figure 19
Figure 19: (a) Bedside chest radiograph in a patient with severe hantavirus pulmonary syndrome shows extensive bilateral interstitial opac-
ities. (b) Frontal chest radiograph obtained 6 hours later demonstrates rapid progression to diffuse perihilar and lower lung consolidation,
reflecting associated diffuse alveolar damage. (Images courtesy of Loren Ketai, MD, Albuquerque, NM.)
edema, fibrin, and variable numbers SARS.—SARS caused by SARS- cells, and bronchiolar injury with loss
of inflammatory cells) and proliferative associated coronavirus is a systemic infec- of cilia are other observed features
(eg, proliferation of reparative type II tion that clinically manifests as progres- (136,137). Patients who die after the 10th
pneumocytes, fibroblastic thickening of sive pneumonia (129–131). SARS was first day of illness present with a mixture of
the alveolar septa with severe airspace detected in the Guangdong Province of acute changes and those of the organizing
disorganization, and distortion of lung China in late 2002, with major outbreaks phase of diffuse alveolar damage (19)
architecture) stages of diffuse alveolar in Hong Kong, Guangdong, Singapore, (Fig 5).
damage (18). and Toronto and Vancouver, Canada The imaging features of SARS-asso-
Chest radiographs may be initially (132). More than 8000 people were af- ciated coronavirus infection consist of
normal but progressively worsen, dis- fected, with a mortality rate of 10%. unilateral or bilateral ground-glass opac-
playing signs of pulmonary edema and The typical clinical manifestation of ities, focal unilateral or bilateral areas
acute respiratory distress syndrome SARS-associated coronavirus includes of consolidation, or a mixture of both.
(125,126). The findings at chest radi- an incubation period of 2–10 days, early In the areas of ground-glass opacifica-
ography may represent differences in systemic symptoms followed within 2–7 tion, thickening of the intralobular in-
the extent of alveolar epithelial dam- days by dry cough or shortness of breath, terstitium or interlobular septa may be
age seen in hantavirus pulmonary syn- the development of radiographically con- present (Fig 20). If marked septal thick-
drome and acute respiratory distress firmed pneumonia by day 7–10, and, in ening occurs, a crazy-paving appear-
syndrome (127). The lack of peripheral many cases, lymphocytopenia (133,134). ance results (134,138–141). Cavitation,
distribution of initial airspace disease, Criteria for the confirmation of SARS calcification, a reticular or nodular pat-
the prominence of interstitial edema, at laboratory analysis include detection tern of opacification, lymphadenopathy,
and the presence of pleural effusions of antibodies in a convalescent-phase or pleural effusion are not features of
early in the disease process are in con- blood serum sample, detection of SARS- SARS (14).
trast to the typical radiographic findings associated coronavirus in a clinical speci-
in acute respiratory distress syndrome men with reverse transcriptase PCR, or Selected DNA Viruses
(126) (Fig 19). isolation of SARS-associated coronavirus Adenovirus.—Human adenoviruses are
The CT appearances of hantavirus in a cultured clinical specimen (135). nonenveloped, double-stranded DNA
pulmonary syndrome consist of exten- Histologically, acute diffuse alveolar viruses belonging to the family Adeno-
sive bilateral ground-glass opacities, damage with airspace edema is the most viridae. More than 50 serotypes have
thickened interlobular septa, few poorly prominent feature in patients who die been described, and approximately half
defined small nodules, bronchial wall before the 10th day after onset of illness. of these serotypes are known human
thickening, and small bilateral pleural Hyaline membranes, interstitial edema, pathogens. Depending on the serotype,
effusions (128). interstitial infiltrates of inflammatory adenovirus may cause respiratory disease

Figure 20 Figure 21
Figure 20: Transverse thin-section CT scan at the level of the lower

pulmonary veins in a patient with SARS infection shows a focal area of
consolidation in the medial segment of the left lower lobe (arrows) and
bilateral ground-glass opacities in the lower lobes (arrowheads).
(Image courtesy of Nestor L. Müller, MD, Vancouver, Canada.) Figure 21: Transverse thin-section CT scan at end expiration in a
patient with Swyer-James-MacLeod syndrome after adenovirus bron-
chiolitis in childhood shows a decrease in attenuation and vascularity of
(serotypes 1–3 and 7) or other illnesses the right lung; a hyperattenuating zone is also visible in the posterior
such as gastroenteritis, keratoconjunc- left upper lobe. The peripheral pulmonary markings are diminutive
tivitis, cystitis, meningoencephalitis, and as a result of vascular narrowing, and a clear shift of the
hepatitis. Adenoviral infections are more mediastinum to the left is also seen (arrow).
common from fall to spring.
Humans are the reservoir for the chial wall thickening, and bronchiectasis Herpes simplex virus type 1.—
adenoviruses that cause human disease. (14,147,148). Air trapping is commonly Herpes simplex virus type 1 pneumonia
Adenovirus accounts for 5%–10% of visible on expiratory CT scans as areas may be a life-threatening infection seen
acute respiratory infections in infants of low attenuation that represent regions almost exclusively in immunocompro-
and children but for less than 1% of re- of lung that are poorly ventilated and mised and/or mechanically ventilated
spiratory illnesses in adults (142). perfused (146,147,149–151) (Fig 21). patients, usually as a component of poly-
Swyer-James-MacLeod syndrome is Adenovirus infections in immuno- microbial infection (156). Herpes sim-
considered to be an acquired disease sec- compromised individuals (eg, stem cell plex virus pneumonia is rare in patients
ondary to adenovirus infection in child- and solid organ transplant recipients) who have undergone solid organ or he-
hood (143–146). A typical infection pro- are increasingly recognized as substan- matopoietic stem cell transplantation
duces cough, nasal congestion, and coryza tial causes of morbidity and mortality. or those who have received cytotoxic or
and is often accompanied by systemic In the stem cell transplantation popula- immunosuppressive agents. Histologi-
symptoms such as headache, fever, chills, tion, the frequency of disease ranges cally, diagnosis depends on recognition
malaise, and myalgia. from 3% to 47% (152). Adenovirus pneu- of herpes virus cytopathic changes in
In a study by Chang et al (146) of 19 monia has been documented in kidney infected cells (eg, mild nucleomegaly
children with postinfectious bronchioli- and liver transplant recipients (144) and formation of intranuclear viral par-
tis obliterans, chest radiographs showed but has only been sporadically reported ticles that coalesce, forming eosino-
five patterns: (a) unilateral hyperlu- in lung transplant recipients (153). A philic viral inclusions) (Fig 1).
cency of increased volume, (b) complete rapidly fatal adenovirus necrotizing pneu- Umans et al (157) reviewed the ra-
collapse of the affected lobe, (c) unilat- monia, early in the posttransplantation diographic findings in 14 patients with
eral hyperlucency of a small or normal- course, may occur in the pediatric pop- herpes simplex virus pneumonia. The
sized lung, (d) bilateral hyperlucent ulation (153). abnormalities in 12 patients manifested
lungs, and (e) mixed pattern of persis- The radiographic manifestations con- as lung opacification, which was pre-
tent collapse and hyperlucent and peri- sist of patchy bilateral areas of consolida- dominantly lobar or more extensive and
bronchial thickening. Thin-section CT tion in a lobular or segmental distribution always bilateral. Although most patients
findings in postinfectious bronchiolitis and/or bilateral ground-glass opacities had a mixed airspace and interstitial
obliterans consist of sharply marginated with a random distribution (144,154) pattern of opacity, 11 showed at least an
focal areas of increased and decreased (Fig 22). In children, adenovirus may airspace consolidation. Lobar, segmen-
lung opacity with reduced vessel size result in lobar collapse, especially of the tal, or subsegmental atelectasis was pre-
in low-attenuation lung regions, bron- right upper lobe (155). sent in seven patients. Pleural effusions

Figure 22 Figure 23
Figure 22: Transverse thin-section CT scan at the level of the carina

in a patient with adenovirus infection shows combination of bilateral
widespread areas of ground-glass opacity with bilateral subsegmental
areas of consolidation (arrows). (Image courtesy of Kyung Soo Lee, MD, Figure 23: Transverse thin-section CT scan at the level of the bron-
Seoul, Korea.) chus intermedius in a patient with herpesvirus infection shows multiple,
bilateral, and randomly distributed pulmonary nodules surrounded by a
halo of ground-glass opacity (arrows).
Figure 24 virus or acquired immunodeficiency syn-

drome (AIDS) with chickenpox are at
high risk for developing varicella pneu-
monia (161).
The thin-section CT appearances in
varicella pneumonia largely reflect the
multicentric hemorrhage and necrosis
centered on airways (162). Common find-
ings include numerous nodular opac-
ities measuring 5–10 mm in diameter,
some with a surrounding halo of ground-
glass opacity (halo sign), patchy ground-
glass opacities, and coalescence of nod-
ules (162) A miliary distribution may also
occur (162,163). After antiviral chemo-
therapy, imaging findings disappear con-
Figure 24: Transverse thin-section CT scan at the level of the lower lobes in
currently with healing of skin lesions
a patient with healed varicella-zoster infection shows multiple, bilateral, and
randomly distributed well-defined small pulmonary nodules—some of which (162). Occasionally, lesions may calcify
are calcified (arrows). and persist as well-defined, randomly
scattered, 2–3-mm densely calcified nod-
ules (17) (Fig 24).
can also develop during the course of enpox) is a common contagious infection CMV.—CMV is a DNA virus and a
the disease (34,157,158). in childhood, with increasing frequency in member of the Herpesviridae family,
Common findings at CT include adults (160). Pneumonia, although rare, which includes varicella-zoster virus,
patchy lobular, subsegmental, or seg- is the most serious complication af- herpes simplex virus types 1 and 2, and
mental consolidation and ground-glass fecting adults with chickenpox. Varicella EBV. It is a widely distributed human
opacities; associated small centrilob- pneumonia is estimated to occur in one pathogen and has the capacity to remain
ular nodules and tree-in-bud pattern of every 400 cases of adulthood chick- latent in a variety of nucleated cells. CMV
have been described in patients in- enpox infections, being more common does not produce clinical disease in most
fected with herpes simplex virus type 2 in pregnant and immunosuppressed pa- people with an intact immune system.
(159) (Fig 23). tients (16). CMV pneumonia is a major cause of
Varicella virus.—Varicella virus Predisposing conditions include un- morbidity and mortality following he-
(varicella-zoster virus) is a double- derlying leukemia and lymphoma and matopoietic stem cell and solid organ
stranded DNA virus and a member of other causes of immunodeficiency. Pa- transplantation and in patients with AIDS
the Herpesviridae family. Varicella (chick- tients with human immunodeficiency in whom CD4 cells are decreased to

Figure 25 Figure 26
Figure 26: Close-up view of transverse thin-

section CT scan obtained with a multidetector unit in
a young patient with tracheobronchial papillomatosis
Figure 25: Coronal thin-section CT scan obtained with a multidetector shows a small nodule (papilloma) arising from the
unit in a 41-year-old man with CMV infection after hematopoietic stem tracheal wall (arrowhead). A thin-walled cyst is also
cell transplantation shows multiple, bilateral, and randomly distributed visible in the right upper lobe (arrow). (Image cour-
small ill-defined pulmonary nodules, some of which are surrounded by a tesy of Kyung Soo Lee, MD, Seoul, Korea.)
halo of ground-glass opacity (arrow). Note the presence of multiple small
branch opacities representing cellular bronchiolitis (arrowheads). (Image
courtesy of Dante L. Escuissato, MD, Curitiba, Brazil.) pharyngitis, and lymphadenopathy–which
are often accompanied by splenomegaly
fewer than 100 cells per cubic millime- lobar consolidation, diffuse and focal (174). EBV pneumonia is rare either
ter. CMV infection occurs in up to 70% ground-glass opacities, irregular reticu- in immunocompetent or immunocom-
of bone marrow transplant recipients, lar opacities, and multiple miliary nodules promised subjects. Mild, asymptomatic
and approximately one-third develop or small nodules with associated areas pneumonitis occurs in about 5%–10%
CMV pneumonia (164). This complica- of ground-glass opacity (halo sign) (164, of cases of infectious mononucleosis
tion characteristically occurs during the 169–172) (Fig 25). (174,175).
postengraftment period (30–100 days Nevertheless, the findings of CMV EBV has also been associated with
after transplantation), with a median on- infection in patients with AIDS seem the development of Burkitt lymphoma,
set time of 50–60 days after transplan- to differ from those in patients without Hodgkin lymphoma, nasopharyngeal car-
tation (165,166). AIDS (171). McGuinness et al (173) de- cinoma, and other EBV-associated dis-
Although CMV antigenemia assay has scribed the thin-section CT findings in eases such as EBV-associated hemophago-
been a major advance in the diagnosis 21 patients with AIDS and CMV pneu- cytic lymphoproliferative syndrome and
of CMV infection in organ transplanta- monia. The most common abnormal- chronic active EBV infection (176).
tion (167), recent evaluations of reverse ities consisted of ground-glass opacity, The CT manifestations of EBV pneu-
transcriptase PCR have revealed that consolidation, and discrete pulmonary monia are similar to those of other viral
PCR and antigenemia assay could pro- nodules or masses that measure be- pneumonias. The findings usually consist
vide false-negative results when virus tween 1 and 3 cm. These investigators of lobar consolidation, diffuse and focal
levels are quite low (168). pointed out that the possibility of CMV parenchymal haziness, irregular reticular
Histologically, CMV has four major pneumonia should be considered in pa- opacities, and multiple miliary nodules
patterns of lung involvement: (a) mili- tients with AIDS, particularly if they have or small nodules with associated areas
ary pattern, (b) diffuse interstitial pneu- Kaposi sarcoma and areas of dense con- of ground-glass opacity (halo sign).
monitis, (c) hemorrhagic pneumonia, solidation or masslike opacities. Although Human papilloma virus.—Human pap-
and (d) CMV inclusions associated with consolidation is also relatively com- illoma virus is a double-stranded DNA
minimal inflammation of lung injury. monly seen in patients without AIDS, it virus that only infects humans. Recur-
Because of the obvious overlap in is not dense and does not result in mass- rent respiratory papillomatosis is often
terms of pathologic characteristics, it is like opacities (173). associated with human papilloma virus
not surprising that the thin-section CT EBV.—EBV is a ubiquitous human types 6 and 11. The papillomas may be
findings for each pattern will vary and herpesvirus with worldwide distribution. multiple (tracheobronchial papillomatosis)
be modulated by the exact nature of Primary infection with EBV occurs early and involve the lung parenchyma. The
the underlying pathologic condition. CT in life and manifests as infectious mono- characteristic radiographic manifestations
features of CMV pneumonia consist of nucleosis with the typical triad of fever, consist of bilateral, multiple thin-walled

cysts and nodules. On CT scans, cysts immunocompromised adults. Chest 2004; severe acute respiratory syndrome (SARS).
are round or irregular in shape and usu- 125(4):1343–1351. Histopathology 2004;45(2):119–124.
ally less than 5 cm in diameter; cysts usu- 5. Sullivan CJ, Jordan MC. Diagnosis of viral 20. Kim EA, Lee KS, Primack SL, et al. Viral
ally show smooth but asymmetric thick pneumonia. Semin Respir Infect 1988; pneumonias in adults: radiologic and
walls (2–3 mm) (177,178) (Fig 26). The 3(2):148–161. pathologic findings. RadioGraphics 2002;
22(Spec Issue):S137–S149.
papillomas, either nodules or masses, of- 6. Daum LT, Canas LC, Arulanandam BP,
ten have lobulated margins and measure Niemeyer D, Valdes JJ, Chambers JP. Real- 21. Hall CB. Respiratory syncytial virus and
less than 3 cm in diameter (179). time RT-PCR assays for type and subtype parainfluenza virus. N Engl J Med 2001;
detection of influenza A and B viruses. In- 344(25):1917–1928.
fluenza Other Respir Viruses 2007;1(4):
22. Penn CC, Liu C. Bronchiolitis following in-
167–175.
Conclusion fection in adults and children. Clin Chest
7. Virkki R, Juven T, Mertsola J, Ruuskanen O. Med 1993;14(4):645–654.
Imaging and clinical manifestations of
Radiographic follow-up of pneumonia in
viral pneumonia are not reliably predic- children. Pediatr Pulmonol 2005;40(3):
23. Kim CK, Kim SW, Kim JS, et al. Bronchioli-
tive of its origin. Herein, emphasis was tis obliterans in the 1990s in Korea and the
223–227.
United States. Chest 2001;120(4):1101–1106.
placed on the commonest imaging fea-
8. Copley SJ. Application of computed tomog-
tures of some of the most common vi- raphy in childhood respiratory infections.
24. Johnson BA, Iacono AT, Zeevi A, McCurry
ruses that produce pulmonary disease. KR, Duncan SR. Statin use is associated
Br Med Bull 2002;61:263–279.
with improved function and survival of
Thin-section CT is an effective diag- 9. Shelhamer JH, Gill VJ, Quinn TC, et al. The lung allografts. Am J Respir Crit Care Med
nostic method when findings at chest laboratory evaluation of opportunistic pul- 2003;167(9):1271–1278.
radiography are normal or inconclusive. monary infections. Ann Intern Med 1996;
Although the radiologic manifestations 124(6):585–599. 25. Anderson LJ, Patriarca PA, Hierholzer JC,
Noble GR. Viral respiratory illnesses. Med
of viral pneumonia are nonspecific and 10. Cuchacovich R. Clinical applications of the Clin North Am 1983;67(5):1009–1030.
difficult to differentiate from those of polymerase chain reaction: an update. Infect
other infections, it is important to con- Dis Clin North Am 2006;20(4):735–758, v. 26. Templeton KE, Scheltinga SA, Beersma MF,
Kroes AC, Claas EC. Rapid and sensitive
sider viral infection when confronted 11. Torres HA, Aguilera E, Safdar A, et al. Fatal method using multiplex real-time PCR for
with a rapidly progressive pneumonia cytomegalovirus pneumonia in patients with diagnosis of infections by influenza A and in-
in patients with risk factors for infec- haematological malignancies: an autopsy- fluenza B viruses, respiratory syncytial virus,
tion. Although definitive diagnosis can- based case-control study. Clin Microbiol and parainfluenza viruses 1, 2, 3, and 4.
not be made on the basis of imaging Infect 2008;14(12):1160–1166. J Clin Microbiol 2004;42(4):1564–1569.
features alone, a combination of clinical 12. Aherne W, Bird T, Court SD, Gardner PS, 27. Fox JD. Nucleic acid amplification tests
and radiographic findings can substan- McQuillin J. Pathological changes in virus for detection of respiratory viruses. J Clin
infections of the lower respiratory tract in Virol 2007;40(suppl 1):S15–S23.
tially improve the accuracy of diagnosis
children. J Clin Pathol 1970;23(1):7–18.
in this disease. 28. Aslanzadeh J, Zheng X, Li H, et al. Pro-
Future challenges include a greater 13. Becroft DM. Histopathology of fatal adeno- spective evaluation of rapid antigen tests
virus infection of the respiratory tract in
insight into the appropriate timing and for diagnosis of respiratory syncytial virus
young children. J Clin Pathol 1967;20(4): and human metapneumovirus infections.
indication of imaging studies, determi- 561–569. J Clin Microbiol 2008;46(5):1682–1685.
nation of the relative value of imaging
14. Becroft DM. Bronchiolitis obliterans, bron-
versus molecular analysis for the diag- 29. Pabbaraju K, Tokaryk KL, Wong S, Fox JD.
chiectasis, and other sequelae of adenovi- Comparison of the Luminex xTAG respira-
nosis of viral infections, and an evalua- rus type 21 infection in young children. tory viral panel with in-house nucleic acid
tion of the effect of surveillance imaging J Clin Pathol 1971;24(1):72–82. amplification tests for diagnosis of respira-
on patient outcome. tory virus infections. J Clin Microbiol 2008;
15. Nash G, Foley FD. Herpetic infection of the
middle and lower respiratory tract. Am J 46(9):3056–3062.
Clin Pathol 1970;54(6):857–863. 30. Teba L. Polymerase chain reaction: a new
References
16. Mohsen AH, McKendrick M. Varicella pneu- chapter in critical care diagnosis. Crit Care
1. Greenberg SB. Respiratory viral infections monia in adults. Eur Respir J 2003;21(5): Med 1999;27(5):860–861.
in adults. Curr Opin Pulm Med 2002;8(3): 886–891.
31. Lo YM, Mehal WZ, Fleming KA. False-
201–208.
17. Brunton FJ, Moore ME. A survey of pul- positive results and the polymerase chain
2. Parienti JJ, Carrat F. Viral pneumonia and monary calcification following adult chicken- reaction. Lancet 1988;2(8612):679.
respiratory sepsis: association, causation, pox. Br J Radiol 1969;42(496):256–259.
32. Kotloff RM, Ahya VN, Crawford SW. Pul-
or it depends? Crit Care Med 2007;35(2):
18. Colby TV, Zaki SR, Feddersen RM, Nolte KB. monary complications of solid organ and
639–640.
Hantavirus pulmonary syndrome is distin- hematopoietic stem cell transplantation.
3. Marcos MA, Esperatti M, Torres A. Viral guishable from acute interstitial pneu- Am J Respir Crit Care Med 2004;170(1):
pneumonia. Curr Opin Infect Dis 2009; monia. Arch Pathol Lab Med 2000;124(10): 22–48.
22(2):143–147. 1463–1466.
33. Demirkazik FB, Akin A, Uzun O, Akpinar
4. de Roux A, Marcos MA, Garcia E, et al. 19. Cheung OY, Chan JW, Ng CK, Koo CK. MG, Ariyürek MO. CT findings in immu-
Viral community-acquired pneumonia in non- The spectrum of pathological changes in nocompromised patients with pulmonary

infections. Diagn Interv Radiol 2008;14(2): lung, airway, and vascular diseases as a culous therapy. Radiology 1993 ; 186 ( 3):
75–82. cause. Radiology 1997;205(2):465–470. 653–660.
34. Aquino SL, Dunagan DP, Chiles C, Haponik 46. Remy-Jardin M, Remy J, Gosselin B, Copin 60. Hartman TE, Swensen SJ, Williams DE.
EF. Herpes simplex virus 1 pneumonia: pat- MC, Wurtz A, Duhamel A. Sliding thin slab, Mycobacterium avium-intracellulare com-
terns on CT scans and conventional chest minimum intensity projection technique in plex: evaluation with CT. Radiology 1993;
radiographs. J Comput Assist Tomogr 1998; the diagnosis of emphysema: histopathologic- 187(1):23–26.
22(5):795–800. CT correlation. Radiology 1996;200(3):
61. Itoh H, Tokunaga S, Asamoto H, et al.
665–671.
35. Gulati M, Kaur R, Jha V, Venkataramu NK, Radiologic-pathologic correlations of small
Gupta D, Suri S. High-resolution CT in re- 47. Stern EJ, Müller NL, Swensen SJ, Hartman lung nodules with special reference to peri-
nal transplant patients with suspected pul- TE. CT mosaic pattern of lung attenuation: bronchiolar nodules. AJR Am J Roentgenol
monary infections. Acta Radiol 2000;41(3): etiologies and terminology. J Thorac Imag- 1978;130(2):223–231.
237–241. ing 1995;10(4):294–297.
62. Lee KS, Kim YH, Kim WS, Hwang SH,
36. Franquet T. Imaging of pneumonia: trends 48. Stern EJ, Swensen SJ, Hartman TE, Frank Kim PN, Lee BH. Endobronchial tubercu-
and algorithms. Eur Respir J 2001;18(1): MS. CT mosaic pattern of lung attenuation: losis: CT features. J Comput Assist Tomogr
196–208. distinguishing different causes. AJR Am J 1991;15(3):424–428.
Roentgenol 1995;165(4):813–816. 63. Taubenberger JK, Reid AH, Krafft AE,
37. Franquet T, Müller NL, Giménez A, Martínez
S, Madrid M, Domingo P. Infectious pul- 49. Martin KW, Sagel SS, Siegel BA. Mosaic Bijwaard KE, Fanning TG. Initial genetic
monary nodules in immunocompromised oligemia simulating pulmonary infiltrates characterization of the 1918 “Spanish” in-
patients: usefulness of computed tomogra- on CT. AJR Am J Roentgenol 1986;147(4): fluenza virus. Science 1997;275(5307):
phy in predicting their etiology. J Comput 670–673. 1793–1796.
Assist Tomogr 2003;27(4):461–468. 64. Rothberg MB, Haessler SD, Brown RB.
50. Shah RM, Miller W Jr. Widespread ground-
38. Logan PM, Primack SL, Staples C, Miller glass opacity of the lung in consecutive Complications of viral influenza. Am J Med
RR, Müller NL. Acute lung disease in the patients undergoing CT: does lobular distri- 2008;121(4):258–264.
immunocompromised host: diagnostic ac- bution assist diagnosis? AJR Am J Roent- 65. Oikonomou A, Müller NL, Nantel S. Radio-
curacy of the chest radiograph. Chest 1995; genol 2003;180(4):965–968. graphic and high-resolution CT findings of
108(5):1283–1287. influenza virus pneumonia in patients with
51. Erasmus JJ, McAdams HP, Rossi SE. High-
39. Heussel CP, Kauczor HU, Heussel G, resolution CT of drug-induced lung disease. hematologic malignancies. AJR Am J Roent-
Fischer B, Mildenberger P, Thelen M. Early Radiol Clin North Am 2002;40(1):61–72. genol 2003;181(2):507–511.
detection of pneumonia in febrile neutro- 66. Ostapchuk M, Roberts DM, Haddy R.
52. Flaherty KR. High-resolution computed to-
penic patients: use of thin-section CT. AJR Community-acquired pneumonia in infants
mography and the many faces of idiopathic
Am J Roentgenol 1997;169(5):1347–1353. and children. Am Fam Physician 2004;
pulmonary fibrosis. Am J Respir Crit Care
40. Franquet T, Rodriguez S, Martino R, Giménez Med 2008;177(4):367–368. 70(5):899–908.
A, Salinas T, Hidalgo A. Thin-section CT 67. Lahti E, Peltola V, Virkki R, Ruuskanen O.
53. Flaherty KR, Martinez FJ. Nonspecific in-
findings in hematopoietic stem cell trans- Influenza pneumonia. Pediatr Infect Dis J
terstitial pneumonia. Semin Respir Crit
plantation recipients with respiratory virus 2006;25(2):160–164.
Care Med 2006;27(6):652–658.
pneumonia. AJR Am J Roentgenol 2006;
187(4):1085–1090. 54. Silva CI, Churg A, Müller NL. Hypersensitiv- 68. Shlaes DM. Respiratory syncytial virus in-
ity pneumonitis: spectrum of high-resolution fection: an emerging or unappreciated in-
41. Kanne JP, Godwin JD, Franquet T, Escuissato fection? Semin Respir Crit Care Med 2000;
CT and pathologic findings. AJR Am J
DL, Müller NL. Viral pneumonia after he- 21(4):305–311.
Roentgenol 2007;188(2):334–344.
matopoietic stem cell transplantation: high-
resolution CT findings. J Thorac Imaging 55. Gruden JF, Webb WR, Warnock M. Cen- 69. Kuiken T, Taubenberger JK. Pathology of
2007;22(3):292–299. trilobular opacities in the lung on high- human influenza revisited. Vaccine 2008;
resolution CT: diagnostic considerations 26(suppl 4):D59–D66.
42. Müller NL. High-resolution computed tomog-
and pathologic correlation. AJR Am J Roent- 70. Taubenberger JK, Morens DM. The pathol-
raphy of diffuse lung disease. Curr Opin
genol 1994;162(3):569–574. ogy of influenza virus infections. Annu Rev
Radiol 1989;1(1):5–8.
56. Müller NL, Miller RR. Diseases of the bron- Pathol 2008;3:499–522.
43. Müller NL. Differential diagnosis of chronic
chioles: CT and histopathologic findings. 71. Reid AH, Taubenberger JK, Fanning TG.
diffuse infiltrative lung disease on high-
Radiology 1995;196(1):3–12. The 1918 Spanish influenza: integrating his-
resolution computed tomography. Semin
tory and biology. Microbes Infect 2001;3(1):
Roentgenol 1991;26(2):132–142. 57. Murata K, Khan A, Herman PG. Pulmonary
81–87.
parenchymal disease: evaluation with high-
44. Sherrick AD, Swensen SJ, Hartman TE.
resolution CT. Radiology 1989;170(3 Pt 1): 72. Nichols WG, Guthrie KA, Corey L, Boeckh
Mosaic pattern of lung attenuation on CT
629–635. M. Influenza infections after hematopoietic
scans: frequency among patients with pul-
stem cell transplantation: risk factors, mor-
monary artery hypertension of different 58. Murata K, Itoh H, Todo G, et al. Centri-
tality, and the effect of antiviral therapy.
causes. AJR Am J Roentgenol 1997;169(1): lobular lesions of the lung: demonstration
Clin Infect Dis 2004;39(9):1300–1306.
79–82. by high-resolution CT and pathologic cor-
relation. Radiology 1986;161(3):641–645. 73. de Jong MD, Hien TT. Avian influenza A
45. Worthy SA, Müller NL, Hartman TE, Swensen
(H5N1). J Clin Virol 2006;35(1):2–13.
SJ, Padley SP, Hansell DM. Mosaic attenu- 59. Im JG, Itoh H, Shim YS, et al. Pulmonary
ation pattern on thin-section CT scans of tuberculosis: CT findings—early active dis- 74. Uyeki TM. Human infection with highly
the lung: differentiation among infiltrative ease and sequential change with antituber- pathogenic avian influenza A (H5N1) virus:

review of clinical issues. Clin Infect Dis 89. Carr MJ, Gunson R, Maclean A, et al. Devel- 20-year experience. J Infect Dis 2006;
2009;49(2):279–290. opment of a real-time RT-PCR for the detec- 193(3):387–395.
tion of swine-lineage influenza A (H1N1) virus
75. Tran TH, Nguyen TL, Nguyen TD, et al. 102. Hamelin ME, Côté S, Laforge J, et al. Human
infections. J Clin Virol 2009;45(3):196–199.
Avian influenza A (H5N1) in 10 patients metapneumovirus infection in adults with
in Vietnam. N Engl J Med 2004;350(12): 90. Whiley DM, Bialasiewicz S, Bletchly C, community-acquired pneumonia and ex-
1179–1188. et al. Detection of novel influenza A(H1N1) acerbation of chronic obstructive pulmo-
virus by real-time RT-PCR. J Clin Virol nary disease. Clin Infect Dis 2005;41(4):
76. Qureshi NR, Hien TT, Farrar J, Gleeson FV.
2009;45(3):203–204. 498–502.
The radiologic manifestations of H5N1 avian
influenza. J Thorac Imaging 2006;21(4): 91. Ajlan AMQB, Quiney B, Nicolaou S, Müller 103. Johnstone J, Majumdar SR, Fox JD, Marrie
259–264. NL. Swine-origin influenza A (H1N1) viral TJ. Human metapneumovirus pneumonia
infection: radiographic and CT findings. AJR in adults: results of a prospective study.
77. Subbarao K, Klimov A, Katz J, et al. Char-
Am J Roentgenol 2009;193(6):1494–1499. Clin Infect Dis 2008;46(4):571–574.
acterization of an avian influenza A (H5N1)
virus isolated from a child with a fatal re- 92. Reichman RC, Dolin R. Viral pneumonias. 104. Kamboj M, Gerbin M, Huang CK, et al.
spiratory illness. Science 1998;279(5349): Med Clin North Am 1980;64(3):491–506. Clinical characterization of human meta-
393–396. pneumovirus infection among patients with
93. Chien JW, Johnson JL. Viral pneumonias:
cancer. J Infect 2008;57(6):464–471.
78. Chan PK. Outbreak of avian influenza epidemic respiratory viruses. Postgrad Med
A(H5N1) virus infection in Hong Kong in 2000;107(3):41–42, 45–47, 51–52. 105. Franquet T, Rodríguez S, Martino R, Salinas
1997. Clin Infect Dis 2002;34(suppl 2): T, Giménez A, Hidalgo A. Human meta-
94. Ferguson PE, Sorrell TC, Bradstock KF,
S58–S64. pneumovirus infection in hematopoietic stem
Carr P, Gilroy NM. Parainfluenza virus
cell transplant recipients: high-resolution
79. Wong SS, Yuen KY. Avian influenza virus type 3 pneumonia in bone marrow trans-
computed tomography findings. J Comput
infections in humans. Chest 2006;129(1): plant recipients: multiple small nodules in
Assist Tomogr 2005;29(2):223–227.
156–168. high-resolution lung computed tomography
scans provide a radiological clue to diagno- 106. Rima BK, Duprex WP. Morbilliviruses and
80. Writing Committee of the Second World
sis. Clin Infect Dis doi:10.1086/597297. Pub- human disease. J Pathol 2006;208(2):
Health Organization Consultation on Clini-
lished online February 17, 2009. Accessed 199–214.
cal Aspects of Human Infection with Avian
February 19, 2009.
Influenza A (H5N1) Virus, Abdel-Ghafar 107. Gremillion DH, Crawford GE. Measles pneu-
AN, Chotpitayasunondh T, et al. Update on 95. Simmonds A, Munoz J, Montecalvo M, monia in young adults: an analysis of 106
avian influenza A (H5N1) virus infection in Clones B, Lagamma EF. Outbreak of para- cases. Am J Med 1981;71(4):539–542.
humans. N Engl J Med 2008;358(3):261–273. influenza virus type 3 in a neonatal inten-
108. Quinn JL III. Measles pneumonia in an
sive care unit. Am J Perinatol 2009;26(5):
81. Uyeki TM. Global epidemiology of human adult. Am J Roentgenol Radium Ther Nucl
361–364.
infections with highly pathogenic avian Med 1964;91:560–563.
influenza A (H5N1) viruses. Respirology 96. Weinberg GA, Hall CB, Iwane MK, et al.
109. Young LW, Smith DI, Glasgow LA. Pneu-
2008;13(suppl 1):S2–S9. Parainfluenza virus infection of young chil-
monia of atypical measles: residual nodu-
dren: estimates of the population-based
82. Chotpitayasunondh T, Ungchusak K, lar lesions. Am J Roentgenol Radium Ther
burden of hospitalization. J Pediatr 2009;
Hanshaoworakul W, et al. Human disease Nucl Med 1970;110(3):439–448.
154(5):694–699.
from influenza A (H5N1), Thailand, 2004.
110. Nakanishi M, Okamura S, Demura Y,
Emerg Infect Dis 2005;11(2):201–209. 97. Sinaniotis CA. Viral pneumoniae in chil-
Ishizaki T, Miyamori I, Itou H. HRCT find-
dren: incidence and aetiology. Paediatr Re-
83. Chowell G, Bertozzi SM, Colchero MA, ings for four cases of measles pneumonia
spir Rev 2004;5(suppl A):S197–S200.
et al. Severe respiratory disease concur- [in Japanese]. Nihon Kokyuki Gakkai Zasshi
rent with the circulation of H1N1 influenza. 98. Gasparetto EL, Escuissato DL, Marchiori E, 2001;39(7):466–470.
N Engl J Med 2009;361(7):674–679. Ono S, Frare e Silva RL, Müller NL. High-
111. de Witte L, Abt M, Schneider-Schaulies S,
resolution CT findings of respiratory syncy-
84. Butler D. Swine flu goes global. Nature 2009; van Kooyk Y, Geijtenbeek TB. Measles virus
tial virus pneumonia after bone marrow trans-
458(7242):1082–1083. targets DC-SIGN to enhance dendritic cell
plantation. AJR Am J Roentgenol 2004;
infection. J Virol 2006;80(7):3477–3486.
85. Cohen J. Swine flu outbreak. Out of Mexico? 182(5):1133–1137.
Scientists ponder swine flu’s origins. Science 112. Johnson KM, Bloom HH, Forsyth B, Mufson
99. Williams JV, Martino R, Rabella N, et al. A
2009;324(5928):700–702. MA, Webb PA, Chanock RM. The role of
prospective study comparing human meta-
enteroviruses in respiratory disease. Am
86. Perez-Padilla R, de la Rosa-Zamboni D, pneumovirus with other respiratory viruses
Rev Respir Dis 1963;88(suppl):240–245.
Ponce de Leon S, et al. Pneumonia and re- in adults with hematologic malignancies
spiratory failure from swine-origin influenza and respiratory tract infections. J Infect 113. Boyd MT, Jordan SW, Davis LE. Fatal pneu-
A (H1N1) in Mexico. N Engl J Med 2009; Dis 2005;192(6):1061–1065. monitis from congenital echovirus type 6
361(7):680–689. infection. Pediatr Infect Dis J 1987;6(12):
100. Williams JV, Harris PA, Tollefson SJ, et al.
1138–1139.
87. Cohen J, Enserink M. Swine flu: after de- Human metapneumovirus and lower respi-
lays, WHO agrees—the 2009 pandemic has ratory tract disease in otherwise healthy 114. Toce SS, Keenan WJ. Congenital echovirus
begun. Science 2009;324(5934):1496–1497. infants and children. N Engl J Med 2004; 11 pneumonia in association with pulmo-
350(5):443–450. nary hypertension. Pediatr Infect Dis J
88. World Health Organization. Global alert
1988;7(5):360–362.
and response (GAR): Pandemic (H1N1) 2009. 101. Williams JV, Wang CK, Yang CF, et al. The
http://www.who.int/csr/disease/swineflu role of human metapneumovirus in upper 115. Cheeseman SH, Hirsch MS, Keller EW,
/en/. Accessed April 29, 2009. respiratory tract infections in children: a Keim DE. Fatal neonatal pneumonia caused

by echovirus type 9. Am J Dis Child 1977; 128. Gasparetto EL, Davaus T, Escuissato DL, 141. Paul NS, Roberts H, Butany J, et al. Radio-
131(10):1169. Marchiori E. Hantavirus pulmonary syn- logic pattern of disease in patients with
drome: high-resolution CT findings in one severe acute respiratory syndrome: the
116. Schieble JH, Fox VL, Lennette EH. A prob-
patient. Br J Radiol 2007;80(949):e21–e23. Toronto experience. RadioGraphics 2004;
able new human picornavirus associated
24(2):553–563.
with respiratory diseases. Am J Epidemiol 129. Ketai L, Paul NS, Wong KT. Radiology of
1967;85(2):297–310. severe acute respiratory syndrome (SARS): 142. Chen HL, Chiou SS, Hsiao HP, et al. Respi-
the emerging pathologic-radiologic corre- ratory adenoviral infections in children: a
117. Watanabe T. HTLV-1-associated diseases.
lates of an emerging disease. J Thorac Im- study of hospitalized cases in southern Tai-
Int J Hematol 1997;66(3):257–278.
aging 2006;21(4):276–283. wan in 2001–2002. J Trop Pediatr 2004;
118. Sugimoto M, Kitaichi M, Ikeda A, Nagai S, 50(5):279–284.
130. Peiris JS, Yuen KY, Osterhaus AD, Stöhr K.
Izumi T. Chronic bronchioloalveolitis asso-
The severe acute respiratory syndrome. 143. Myers GD, Bollard CM, Wu MF, et al. Re-
ciated with human T-cell lymphotrophic
N Engl J Med 2003;349(25):2431–2441. constitution of adenovirus-specific cell-
virus type I infection. Curr Opin Pulm Med
mediated immunity in pediatric patients
1998;4(2):98–102. 131 . Muller MP, McGeer A. Severe acute respi-
after hematopoietic stem cell transplanta-
ratory syndrome (SARS) coronavirus. Semin
119. Poiesz BJ, Ruscetti FW, Gazdar AF, Bunn PA, tion. Bone Marrow Transplant 2007;39(11):
Respir Crit Care Med 2007;28(2):201–212.
Minna JD, Gallo RC. Detection and isola- 677–686.
tion of type C retrovirus particles from 132. Centers for Disease Control and Prevention
144. Chong S, Lee KS, Kim TS, Chung MJ,
fresh and cultured lymphocytes of a patient (CDC). Outbreak of severe acute respira-
Chung MP, Han J. Adenovirus pneumonia
with cutaneous T-cell lymphoma. Proc Natl tory syndrome—worldwide, 2003. MMWR
in adults: radiographic and high-resolution
Acad Sci U S A 1980;77(12):7415–7419. Morb Mortal Wkly Rep 2003 ;52 (11):
CT findings in five patients. AJR Am J
226–228. [Published correction appears
120. Kompoliti A, Gage B, Sharma L, Daniels Roentgenol 2006;186(5):1288–1293.
in MMWR Morb Mortal Wkly Rep 2003;
JC. Human T-cell lymphotropic virus type
52(13):284.] 145. Müller NL. Unilateral hyperlucent lung:
1–associated myelopathy, Sjögren syndrome,
MacLeod versus Swyer-James. Clin Radiol
and lymphocytic pneumonitis. Arch Neurol 133. Peiris JS, Chu CM, Cheng VC, et al. Clini-
2004;59(11):1048.
1996;53(9):940–942. cal progression and viral load in a commu-
nity outbreak of coronavirus-associated SARS 146. Chang AB, Masel JP, Masters B. Post-
121. Okada F, Ando Y, Yoshitake S, et al. Pulmo-
pneumonia: a prospective study. Lancet infectious bronchiolitis obliterans: clinical,
nary CT findings in 320 carriers of human
2003;361(9371):1767–1772. radiological and pulmonary function se-
T-lymphotropic virus type 1. Radiology 2006;
quelae. Pediatr Radiol 1998;28(1):23–29.
240(2):559–564. 134. Antonio GE, Wong KT, Hui DS, et al. Thin-
section CT in patients with severe acute re- 147. Marti-Bonmati L, Ruiz Perales F, Catala F,
122. Duchin JS, Koster FT, Peters CJ, et al.
spiratory syndrome following hospital dis- Mata JM, Calonge E. CT findings in Swyer-
Hantavirus pulmonary syndrome: a clinical
charge: preliminary experience. Radiology James syndrome. Radiology 1989;172(2):
description of 17 patients with a newly recog-
2003;228(3):810–815. 477–480.
nized disease. The Hantavirus Study Group.
N Engl J Med 1994;330(14):949–955. 135. Guidelines for laboratory diagnosis of SARS- 148. Lynch DA, Brasch RC, Hardy KA, Webb WR.
CoV infection. Centers for Disease Control Pediatric pulmonary disease: assessment
123. Khan AS, Khabbaz RF, Armstrong LR, et al.
and Prevention Web site. http://www.cdc with high-resolution ultrafast CT. Radiology
Hantavirus pulmonary syndrome: the first
.go/ncidod/sars/lab.htm. Accessed May 3, 1990;176(1):243–248.
100 US cases. J Infect Dis 1996 ; 173( 6 ):
2005.
1297–1303. 149. Lucaya J, Gartner S, García-Peña P, Cobos N,
136. Hwang DM, Chamberlain DW, Poutanen Roca I, Liñan S. Spectrum of manifestations
124. Cleri DJ, Ricketti AJ, Porwancher RB,
SM, Low DE, Asa SL, Butany J. Pulmonary of Swyer-James-MacLeod syndrome. J Com-
Ramos-Bonner LS, Vernaleo JR. Viral
pathology of severe acute respiratory syn- put Assist Tomogr 1998;22(4):592–597.
hemorrhagic fevers: current status of en-
drome in Toronto. Mod Pathol 2005;18(1):
demic disease and strategies for control. 150. Stern EJ, Samples TL. Dynamic ultrafast
1–10.
Infect Dis Clin North Am 2006;20(2):359– high resolution CT findings in a case of
393, x. 137. Nicholls JM, Poon LL, Lee KC, et al. Lung Swyer-James syndrome. Pediatr Radiol 1992;
pathology of fatal severe acute respira- 22(5):350–352.
125. Ketai LH, Williamson MR, Telepak RJ, et al.
tory syndrome. Lancet 2003;361(9371):
Hantavirus pulmonary syndrome: radio- 151. Moore AD, Godwin JD, Dietrich PA,
1773–1778.
graphic findings in 16 patients. Radiology Verschakelen JA, Henderson WR Jr. Swyer-
1994;191(3):665–668. 138. Müller NL, Ooi GC, Khong PL, Nicolaou S. James syndrome: CT findings in eight pa-
Severe acute respiratory syndrome: radio- tients. AJR Am J Roentgenol 1992;158(6):
126. Ketai LH, Kelsey CA, Jordan K, et al. Distin-
graphic and CT findings. AJR Am J Roent- 1211–1215.
guishing Hantavirus pulmonary syndrome
genol 2003;181(1):3–8.
from acute respiratory distress syndrome 152. Bruno B, Gooley T, Hackman RC, Davis C,
by chest radiography: are there different 139. Wong KT, Antonio GE, Hui DS, et al. Thin- Corey L, Boeckh M. Adenovirus infection
radiographic manifestations of increased section CT of severe acute respiratory syn- in hematopoietic stem cell transplantation:
alveolar permeability? J Thorac Imaging drome: evaluation of 73 patients exposed to effect of ganciclovir and impact on survival.
1998;13(3):172–177. or with the disease. Radiology 2003;228(2): Biol Blood Marrow Transplant 2003;9(5):
395–400. 341–352.
127. Boroja M, Barrie JR, Raymond GS. Radio-
graphic findings in 20 patients with Hanta- 140. Ooi GC, Khong PL, Müller NL, et al. Severe 153. Ohori NP, Michaels MG, Jaffe R, Williams P,
virus pulmonary syndrome correlated with acute respiratory syndrome: temporal lung Yousem SA. Adenovirus pneumonia in lung
clinical outcome. AJR Am J Roentgenol changes at thin-section CT in 30 patients. transplant recipients. Hum Pathol 1995;
2002;178(1):159–163. Radiology 2004;230(3):836–844. 26(10):1073–1079.

154. Motallebi M, Mukunda BN, Ravakhah K. 167. Razonable RR, Emery VC; 11th Annual man. AJR Am J Roentgenol 1979;132(5):
Adenoviral bronchopneumonia in an im- Meeting of the IHMF (International Herpes 820–822.
munocompetent adult: computed tomogra- Management Forum). Management of CMV
180. Falsey AR, Walsh EE. Viral pneumonia in
phy and pathologic correlations. Am J Med infection and disease in transplant patients.
older adults. Clin Infect Dis 2006;42(4):
Sci 2003;325(5):285–287. 27–29 February 2004. Herpes 2004;11(3):
518–524.
77–86.
155. Chiu CY, Wong KS, Huang YC, Lin TY. Bron-
181 . Camps Serra M, Cervera C, Pumarola T,
chiolitis obliterans in children: clinical pre- 168. Thorne LB, Civalier C, Booker J, Fan H,
et al. Virological diagnosis in community-
sentation, therapy and long-term follow-up. Gulley ML. Analytic validation of a quanti-
acquired pneumonia in immunocompro-
J Paediatr Child Health 2008;44(3):129–133. tative real-time PCR assay to measure CMV
mised patients. Eur Respir J 2008;31(3):
viral load in whole blood. Diagn Mol Pathol
156. Luyt CE, Combes A, Nieszkowska A, 618–624.
2007;16(2):73–80.
Trouillet JL, Chastre J. Viral infections in 182. Lau SK, To WK, Tse PW, et al. Human
the ICU. Curr Opin Crit Care 2008;14(5): 169. Bonatti H, Pruett TL, Brandacher G, et al.
parainfluenza virus 4 outbreak and the
605–608. Pneumonia in solid organ recipients: spec-
role of diagnostic tests. J Clin Microbiol
trum of pathogens in 217 episodes. Trans-
2005;43(9):4515–4521.
157. Umans U, Golding RP, Duraku S, Manoliu RA. plant Proc 2009;41(1):371–374.
Herpes simplex virus 1 pneumonia: con- 183. González Y, Martino R, Rabella N, Labeaga R,
ventional chest radiograph pattern. Eur 170. Nomura F, Shimokata K, Sakai S, Yamauchi
Badell I, Sierra J. Community respiratory
Radiol 2001;11(6):990–994. T, Kodera Y, Saito H. Cytomegalovirus pneu-
virus infections in patients with hematologic
monitis occurring after allogeneic bone
malignancies. Haematologica 1999;84(9):
158. Ramsey PG, Fife KH, Hackman RC, Meyers marrow transplantation: a study of 106 re-
820–823.
JD, Corey L. Herpes simplex virus pneu- cipients. Jpn J Med 1990;29(6):595–602.
monia: clinical, virologic, and pathologic 184. Wendt CH. Community respiratory viruses:
features in 20 patients. Ann Intern Med 171 . Moon JH, Kim EA, Lee KS, Kim TS, Jung organ transplant recipients. Am J Med
1982;97(6):813–820. KJ, Song JH. Cytomegalovirus pneumonia: 1997;102(3A):31–36, discussion 42–43.
high-resolution CT findings in ten non-AIDS
159. Gasparetto EL, Escuissato DL, Inoue C, immunocompromised patients. Korean J 185. Castagnola E, Cappelli B, Erba D, Rabagliati
Marchiori E, Müller NL. Herpes simplex Radiol 2000;1(2):73–78. A, Lanino E, Dini G. Cytomegalovirus in-
virus type 2 pneumonia after bone marrow fection after bone marrow transplanta-
172. Franquet T, Lee KS, Müller NL. Thin-section tion in children. Hum Immunol 2004;65(5):
transplantation: high-resolution CT findings
CT findings in 32 immunocompromised pa- 416–422.
in 3 patients. J Thorac Imaging 2005;20(2):
tients with cytomegalovirus pneumonia who
71–73.
do not have AIDS. AJR Am J Roentgenol 186. Konoplev S, Champlin RE, Giralt S, et al.
160. Frangides CY, Pneumatikos I. Varicella- 2003;181(4):1059–1063. Cytomegalovirus pneumonia in adult autolo-
zoster virus pneumonia in adults: report of gous blood and marrow transplant recipi-
173. McGuinness G, Scholes JV, Garay SM, ents. Bone Marrow Transplant 2001;27(8):
14 cases and review of the literature. Eur J
Leitman BS, McCauley DI, Naidich DP. 877–881.
Intern Med 2004;15(6):364–370.
Cytomegalovirus pneumonitis: spectrum of
161 . Popara M, Pendle S, Sacks L, Smego RA Jr, parenchymal CT findings with pathologic 187. Chang GC, Wu CL, Pan SH, et al. The di-
Mer M. Varicella pneumonia in patients correlation in 21 AIDS patients. Radiology agnosis of pneumonia in renal transplant
with HIV/AIDS. Int J Infect Dis 2002;6(1): 1994;192(2):451–459. recipients using invasive and noninvasive
6–8. procedures. Chest 2004;125(2):541–547.
174. Gautschi O, Berger C, Gubler J, Laube I.
Acute respiratory failure and cerebral hem- 188. Aisenberg GM, Torres HA, Tarrand J, Safdar
162. Kim JS, Ryu CW, Lee SI, Sung DW, Park
orrhage due to primary Epstein-Barr virus A, Bodey G, Chemaly RF. Herpes simplex
CK. High-resolution CT findings of varicella-
infection. Respiration 2003;70(4):419–422. virus lower respiratory tract infection in
zoster pneumonia. AJR Am J Roentgenol
patients with solid tumors. Cancer 2009;
1999;172(1):113–116. 175. Teira P, Agbalika F, Bergeron A, et al. Primary 115(1):199–206.
163. Maher TM, Gupta NK, Burke MM, Carby Epstein-Barr virus infection with pneumonia
transmitted by allogeneic bone marrow 189. Whimbey E, Champlin RE, Couch RB, et al.
MR. CT findings of varicella pneumonia
after transplantation. Clin Infect Dis 2006; Community respiratory virus infections
after lung transplantation. AJR Am J Roent-
43(7):892–895. among hospitalized adult bone marrow
genol 2007;188(6):W557–W559.
transplant recipients. Clin Infect Dis 1996;
176. Kutok JL, Wang F. Spectrum of Epstein- 22(5):778–782.
164. Gasparetto EL, Ono SE, Escuissato D, et al.
Barr virus–associated diseases. Annu Rev
Cytomegalovirus pneumonia after bone mar- 190. Thompson WW, Comanor L, Shay DK.
Pathol 2006;1:375–404.
row transplantation: high-resolution CT find- Epidemiology of seasonal influenza: use of
ings. Br J Radiol 2004;77(921):724–727. 177. Kramer SS, Wehunt WD, Stocker JT, surveillance data and statistical models to
Kashima H. Pulmonary manifestations of estimate the burden of disease. J Infect Dis
165. Kang EY, Patz EF Jr, Müller NL. Cytomeg-
juvenile laryngotracheal papillomatosis. AJR 2006;194(suppl 2):S82–S91.
alovirus pneumonia in transplant patients:
Am J Roentgenol 1985;144(4):687–694.
CT findings. J Comput Assist Tomogr 1996; 191 . Bowton DL, Bass DA. Community-acquired
20(2):295–299. 178. Zawadzka-Głos L, Jakubowska A, Chmielik M, pneumonia: the clinical dilemma. J Thorac
Bielicka A, Brzewski M. Lower airway pap- Imaging 1991;6(3):1–5.
166. Worthy SA, Flint JD, Müller NL. Pulmo-
illomatosis in children. Int J Pediatr Otorhi-
nary complications after bone marrow 192. Jennings LC, Anderson TP, Beynon KA,
nolaryngol 2003;67(10):1117–1121.
transplantation: high-resolution CT and et al. Incidence and characteristics of viral
pathologic findings. RadioGraphics 1997; 179. Glazer G, Webb WR. Laryngeal papilloma- community-acquired pneumonia in adults.
17(6):1359–1371. tosis with pulmonary spread in a 69-year-old Thorax 2008;63(1):42–48.

193. Mandell LA, Bartlett JG, Dowell SF, et al. 206. Crowe JE Jr. Human metapneumovirus as 221. Hogg JC. Infection and COPD. Exp Lung
Update of practice guidelines for the man- a major cause of human respiratory tract dis- Res 2005;31(suppl 1):72–73.
agement of community-acquired pneumonia ease. Pediatr Infect Dis J 2004;23(11 suppl): 222. Papi A, Bellettato CM, Braccioni F, et al.
in immunocompetent adults. Clin Infect Dis S215–S221. Infections and airway inflammation in chronic
2003;37(11):1405–1433. obstructive pulmonary disease severe ex-
207. Coker R. Swine flu. BMJ 2009;338:b1791.
194. Shapiro JM, Jean RE. Respiratory syncytial acerbations. Am J Respir Crit Care Med
208. Cohen J. Swine flu outbreak: past pandemics
virus. N Engl J Med 2001;345(15):1132–1133. 2006;173(10):1114–1121.
provide mixed clues to H1N1’s next moves.
195. Falsey AR, Walsh EE. Respiratory syncytial Science 2009;324(5930):996–997. 223. Falsey AR, Hennessey PA, Formica MA,
virus infection in adults. Clin Microbiol Rev Cox C, Walsh EE. Respiratory syncytial
209. Beckford-Ball J. Swine flu panic shows how virus infection in elderly and high-risk adults.
2000;13(3):371–384.
little we really care. Br J Nurs 2009;18(9): N Engl J Med 2005;352(17):1749–1759.
196. Schlesinger C, Koss MN. Bronchiolitis: 521.
update 2001. Curr Opin Pulm Med 2002; 224. Seemungal TA, Wedzicha JA. Viral infec-
210 . Greenberg SB. Viral pneumonia. Infect Dis tions in obstructive airway diseases. Curr
8(2):112–116.
Clin North Am 1991;5(3):603–621. Opin Pulm Med 2003;9(2):111–116.
197. Angeles Marcos M, Camps M, Pumarola T,
211 . Macfarlane J, Holmes W, Gard P, et al. 225. Smith CB, Golden CA, Kanner RE, Renzetti
et al. The role of viruses in the aetiology of
Prospective study of the incidence, aetiol- AD Jr. Association of viral and Myco-
community-acquired pneumonia in adults.
ogy and outcome of adult lower respiratory plasma pneumoniae infections with acute
Antivir Ther 2006;11(3):351–359.
tract illness in the community. Thorax 2001; respiratory illness in patients with chronic
198. Mandell LA, Wunderink RG, Anzueto A, et al. 56(2):109–114. obstructive pulmonary diseases. Am Rev
Infectious Diseases Society of America/ Respir Dis 1980;121(2):225–232.
212 . Creer DD, Dilworth JP, Gillespie SH, et al.
American Thoracic Society consensus guide-
Aetiological role of viral and bacterial in- 226. Beckham JD, Cadena A, Lin J, et al. Re-
lines on the management of community-
fections in acute adult lower respiratory spiratory viral infections in patients with
acquired pneumonia in adults. Clin Infect Dis
tract infection (LRTI) in primary care. Tho- chronic, obstructive pulmonary disease.
2007;44(suppl 2):S27–S72.
rax 2006;61(1):75–79. J Infect 2005;50(4):322–330.
199. Bouza E, Muñoz P. Introduction: infections 227. Woodhead M, Blasi F, Ewig S, et al. Guide-
213. Johnstone J, Majumdar SR, Fox JD, Marrie
caused by emerging resistant pathogens. lines for the management of adult lower
TJ. Viral infection in adults hospitalized
Clin Microbiol Infect 2005;11(suppl 4):iv. respiratory tract infections. Eur Respir J
with community-acquired pneumonia: prev-
200. Schwartz DA, Bryan RT, Hughes JM. Pathol- alence, pathogens, and presentation. Chest 2005;26(6):1138–1180.
ogy and emerging infections—quo vadimus? 2008;134(6):1141–1148. 228. Mallia P, Johnston SL. How viral infections
Am J Pathol 1995;147(6):1525–1533. cause exacerbation of airway diseases. Chest
214. Gern JE. Viral respiratory infection and
201 . Cheney PR. Update on emerging infections the link to asthma. Pediatr Infect Dis J 2006;130(4):1203–1210.
from the Centers for Disease Control and Pre- 2008;27(10 suppl):S97–S103. 229. Carroll KN, Hartert TV. The impact of re-
vention. Hantavirus pulmonary syndrome— spiratory viral infection on wheezing ill-
215. Falsey AR. Respiratory syncytial virus in-
Colorado and New Mexico, 1998. Ann nesses and asthma exacerbations. Immu-
fection in adults. Semin Respir Crit Care
Emerg Med 1999;33(1):121–123. nol Allergy Clin North Am 2008;28(3):
Med 2007;28(2):171–181.
539–561, viii.
202. Hammel JM, Chiang WK. Update on emerg-
216. Manoha C, Espinosa S, Aho SL, Huet F,
ing infections: news from the Centers for 230. Jartti T, Lee WM, Pappas T, Evans M,
Pothier P. Epidemiological and clinical fea-
Disease Control and Prevention. Outbreaks Lemanske RF Jr, Gern JE. Serial viral in-
tures of hMPV, RSV and RVs infections in
of avian influenza A (H5N1) in Asia and fections in infants with recurrent respiratory
young children. J Clin Virol 2007;38(3):
interim recommendations for evaluation illnesses. Eur Respir J 2008;32(2):314–320.
221–226.
and reporting of suspected cases—United 231. Bardin PG, Johnston SL, Pattemore PK.
States, 2004. Ann Emerg Med 2005;45(1): 217. Lim WS, Macfarlane JT, Colthorpe CL. Viruses as precipitants of asthma symp-
88–92. Treatment of community-acquired lower re- toms. II. Physiology and mechanisms. Clin
spiratory tract infections during pregnancy. Exp Allergy 1992;22(9):809–822.
203. Cameron PA, Rainer TH. Update on emerg-
Am J Respir Med 2003;2(3):221–233.
ing infections: news from the Centers for 232. Beadling C, Slifka MK. How do viral infec-
Disease Control and Prevention. Update: out- 218. Kumar D, Erdman D, Keshavjee S, et al. tions predispose patients to bacterial infec-
break of severe acute respiratory syndrome— Clinical impact of community-acquired re- tions? Curr Opin Infect Dis 2004;17(3):
worldwide, 2003. Ann Emerg Med 2003; spiratory viruses on bronchiolitis obliter- 185–191.
42(1):110–112. ans after lung transplant. Am J Transplant
233. Corne JM, Marshall C, Smith S, et al. Fre-
2005;5(8):2031–2036.
204. Hamelin ME, Abed Y, Boivin G. Human quency, severity, and duration of rhinovirus
metapneumovirus: a new player among re- 219. Palmer SM Jr, Henshaw NG, Howell DN, infections in asthmatic and non-asthmatic
spiratory viruses. Clin Infect Dis 2004;38(7): Miller SE, Davis RD, Tapson VF. Commu- individuals: a longitudinal cohort study.
983–990. nity respiratory viral infection in adult lung Lancet 2002;359(9309):831–834.
transplant recipients. Chest 1998;113(4):
205. Madhi SA, Ludewick H, Abed Y, Klugman 234. Kim YJ, Boeckh M, Englund JA. Commu-
944–950.
KP, Boivin G. Human metapneumovirus- nity respiratory virus infections in immu-
associated lower respiratory tract infections 220. Hopkins P, McNeil K, Kermeen F, et al. nocompromised patients: hematopoietic
among hospitalized human immunodefi- Human metapneumovirus in lung transplant stem cell and solid organ transplant recipi-
ciency virus type 1 (HIV-1)–infected and recipients and comparison to respiratory ents, and individuals with human immuno-
HIV-1-uninfected African infants. Clin In- syncytial virus. Am J Respir Crit Care Med deficiency virus infection. Semin Respir Crit
fect Dis 2003;37(12):1705–1710. 2008;178(8):876–881. Care Med 2007;28(2):222–242.

235. Hwang EA, Kang MJ, Han SY, Park SB, 242. Lyu DM, Zamora MR. Medical complications the status quo. Clin Transplant 2007;21(2):
Kim HC. Viral infection following kidney of lung transplantation. Proc Am Thorac 149–158.
transplantation: long-term follow-up in a Soc 2009;6(1):101–107.
single center. Transplant Proc 2004;36(7): 250. Saner FH, Olde Damink SW, Pavlakovic G,
243. López-Medrano F, Aguado JM, Lizasoain M, et al. Pulmonary and blood stream infec-
2118–2119.
et al. Clinical implications of respiratory tions in adult living donor and cadaveric
236. Ljungman P. Respiratory virus infections in virus infections in solid organ transplant liver transplant patients. Transplantation
stem cell transplant patients: the European recipients: a prospective study. Transplan- 2008;85(11):1564–1568.
experience. Biol Blood Marrow Transplant tation 2007;84(7):851–856.
2001;7(suppl):5S–7S. 251. Zhang XD, Hu XP, Yin H, et al. Aspergillus
244. Mattner F, Fischer S, Weissbrodt H, et al.
pneumonia in renal transplant recipients.
Post-operative nosocomial infections after
237. Matar LD, McAdams HP, Palmer SM, et al. Chin Med J (Engl) 2008;121(9):791–794.
lung and heart transplantation. J Heart
Respiratory viral infections in lung trans-
Lung Transplant 2007;26(3):241–249. 252. Whimbey E, Ghosh S. Respiratory syncytial
plant recipients: radiologic findings with clin-
ical correlation. Radiology 1999;213(3): 245. Puzio J, Kucewicz E, Sioła M, et al. Atypi- virus infections in immunocompromised
735–742. cal and opportunistic pulmonary infections adults. Curr Clin Top Infect Dis 2000;20:
after cardiac surgery [in Polish]. Anestezjol 232–255.
238. Leung AN, Gosselin MV, Napper CH, et al. Intens Ter 2009;41(1):41–45.
Pulmonary infections after bone marrow 253. Flomenberg P, Babbitt J, Drobyski WR,
transplantation: clinical and radiographic 246. Campos S, Caramori M, Teixeira R, et al. et al. Increasing incidence of adenovirus
findings. Radiology 1999;210(3):699–710. Bacterial and fungal pneumonias after lung disease in bone marrow transplant recipi-
transplantation. Transplant Proc 2008;40(3): ents. J Infect Dis 1994;169(4):775–781.
239. Ison MG, Fishman JA. Cytomegalovirus 822–824.
pneumonia in transplant recipients. Clin 254. Rañó A, Agustí C, Jimenez P, et al. Pulmo-
247. Puchhammer-Stöckl E. Herpesviruses and nary infiltrates in non-HIV immunocom-
Chest Med 2005;26(4):691–705, viii.
the transplanted lung: looking at the air promised patients: a diagnostic approach
240. Bozbas SS, Eyuboglu FO, Ozturk Ergur F, side. J Clin Virol 2008;43(4):415–418. using non-invasive and bronchoscopic pro-
et al. Pulmonary complications and mortality 248. Sund F, Lidehäll AK, Claesson K, et al. CMV- cedures. Thorax 2001;56(5):379–387.
after liver transplant. Exp Clin Transplant specific T-cell immunity, viral load, and
2008;6(4):264–270. 255. Templeton KE, Scheltinga SA, van den
clinical outcome in seropositive renal trans-
Eeden WC, Graffelman AW, van den Broek
plant recipients: a pilot study. Clin Trans-
241. Ng YL, Paul N, Patsios D, et al. Imaging of PJ, Claas EC. Improved diagnosis of the
plant 2010;24(3):401–409.
lung transplantation: review. AJR Am J etiology of community-acquired pneumonia
Roentgenol 2009;192(3 suppl):S1–S13; quiz 249. Fishman JA, Emery V, Freeman R, et al. Cyto- with real-time polymerase chain reaction.
S14–S19. megalovirus in transplantation—challenging Clin Infect Dis 2005;41(3):345–351.

Imaging of Pulmonary Viral Pneumonia: Online CME

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Imaging of Pulmonary Viral

Tomás Franquet, MD, PhD

Learning Objectives: Supplemental material: http://radiology.rsna.org/lookup

Accreditation and Designation Statement

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Figure 1 Figure 2 Figure 3

Figure 2: Histopathologic features of respiratory

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Figure 4 Figure 5 and not invariably associated with pneu-

Laboratory Identification Methods

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Figure 6: Transverse expiratory thin-section CT scan through the

Figure 9: Transverse thin-section CT scan through the lower lobes in a

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Figure 10: Transverse thin-section CT scan through the lower lobes

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Table 2 Avian flu (H5N1).—Avian influenza

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Figure 12: Transverse thin-section CT scan through the upper lobes

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Figure 16: Transverse thin-section CT scan through the upper lobes

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Figure 20: Transverse thin-section CT scan at the level of the lower

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Figure 22: Transverse thin-section CT scan at the level of the carina

Figure 24 virus or acquired immunodeficiency syn-

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Figure 26: Close-up view of transverse thin-

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