Imaging Pulmonary Infection
Prompt detections of imaging studies may nanteffusions(Fig.10),hemothorax,andse
improvepatientcare,enablingcliniciansto
treatpatientswithanappropriatecourseof
antibiotictherapy[27].
Detectionofanairfluidlevelatchestradi
ographyshouldpromptevaluationofitsloca
tionasbeinginthelungparenchymaorwithin
thepleuralspace.Alungabscesswithanair
fluid level can be differentiated from em
pyema with bronchopleural fistula by mea
surementandcomparisonofthelengthsofthe
visualized airfluid level on orthogonal chest
radiographs. Because of the characteristic
sphericalshapeofalungabscess,anassociated
airfluid level typically has equal lengths on
posteroanterior and lateral chest radiographs
(Fig.8).Bycontrast,empyematypicallyforms
lenticularcollectionsofpleuralfluid,andan
associatedairfluidlevel(e.g.,bronchopleural
fistula)usuallyexhibitslengthdisparitywhen
A comparedonposteroanteriorandlateralchest
m radiographs. In addition, both entities
eri typicallydisplayadifferenceintheangleof
ca
theirinterfacewithanadjacentpleuralsurface.
n
Jo Alungabscessusuallyformsanacuteangle
ur when it intersects with an adjacent pleural
na surface, and its wall is often thick and
l signisbranchingendobronchialopacitiesthat
of irregular. By contrast, empyema typically
R forms obtuse angles along its interface with
oe adjacentpleuraandusuallyhassmooth,thin,
nt
enhancing walls [28, 29]. Other differential
ge
no diagnosticconsiderationsforanintrathoracic
lo airfluid level include hemorrhage into a
gy cavity,lungcancer,andmetastaticdisease.
20
14
.2
02 Split-Pleura Sign
:4 Normalvisceralandparietalpleuraarein
79
distinguishableonCTimages.Inthepresence
49 of an exudative pleural effusion with locula
2. tion,inflammatorychangesmaythickenboth
the visceral and parietal pleura that surround
thefluidcollectionandmaybecomeevidentas
thesplitpleurasign,suggestingthepresence
of empyema [28, 30]. A loculated effusion
may have an atypical chest radiographic
appearancewhenlocatedwithinafissure.The
splitpleurasignmaybeseenincombination
withtheairfluidlevelsignwhenabroncho
pleuralfistulaoccurswithinempyema.
Empyema should be considered when a
patient presents with fever, cough, and chest
painandCTshowsthesplitpleurasign.Ina
seriesof58patientswithempyema,thesplit
pleurasignwasseenin68%[30](Fig.9).The
splitpleura sign is not specific for empyema
butratherindicatesthepresenceofanexuda
tive effusion [31]. Other important causes of
thissignincludeparapneumonicandmalig
Air Crescent or Monad Sign
quelae of previous talc pleurodesis, lobecto
my, or pneumonectomy. Hemothorax usually
has associated heterogeneously high attenua
tion,andtalcpleurodesishasattenuationsim
ilartothatofcalciumandisoftenclumped.
Halo Sign
ThehalosignistheCTfindingofaperiph cavity and may exhibit gravity dependence
eralrimofgroundglassopacitysurroundinga
pulmonary nodule or mass [2, 32]. When
detectedinafebrilepatientwithneutropenia,
thissignishighlysuggestiveofangioinvasive
Aspergillus infection [3234] (Fig. 11). The
groundglass opacity represents hemorrhage
surrounding infarcted lung and is caused by
vascularinvasionbythefungus[35].Thehalo
signistypicallyseenearlyinthecourseofthe
infection. In a group of 25 patients with
invasive Aspergillus infection, the halo sign
was seen in 24 patients on day 0 and was
detected in only 19% of patients by day 14,
highlightingtheimportanceofperformingCT
early in the course of a suspected fungal
infection [36]. In a large group of
immunocompromised patients with Asper
gillus infection, Greene and colleagues [37]
foundthatpatientsinwhomthehalosignwas
visualized at CT had improved survival and
response to antifungal treatment compared
with those without the halo sign at CT.
Differential considerations for the halo sign
include other infections, such as mucormy
cosis and Candida (Fig. 12), Pseudomonas,
herpes simplex virus, and cytomegalovirus
infections,andothercauses,suchasWegener
granulomatosis, hemorrhagic metastasis, and
Kaposisarcoma[38,39].
Air Crescent Sign of Angioinvasive
Aspergillus Infection
TheaircrescentsignistheCTfindingofa
crescentic collection of air that separates a
noduleormassfromthewallofasurrounding
cavity [2]. This sign is seen in two types of
Aspergillus infection: angioinvasive and
mycetoma [40]. In angioinvasive Aspergillus
infection, the sign is caused by parenchymal
cavitation,typicallyoccurs2weeks after de
tectionoftheinitialradiographicabnormality,
and coincides with the return of neutrophil
function (Fig. 13). The air crescent sign is
suggestive of a favorable patient prognosis
[41]. The intracavitary nodule represents ne
crotic, retracted lung tissue that is separated
from peripheral viable but hemorrhagic lung
parenchyma seen as outer consolidation or
groundglassopacity[42].
of Mycetoma
Theaircrescentsignofmycetoma,alsore
ferredtoastheMonadsign,isseeninanim
munocompetenthostwithpreexistingcysticor
cavitary lung disease, usually from tuber
culosisorsarcoidosis[42].Thefungalballor
mycetomadevelopswithinapreexistinglung
(Fig.14).Themycetomaiscomposedoffun
gal hyphae, mucus, and cellular debris. My
cetomascancausehemoptysis.Thetreatment
options include surgical resection, bronchial
artery embolization, and instillation of anti
fungalagentsintothecavity[40].Theaircres
centsignisnotspecificfor Aspergillus infec
tionandcanbeseeninotherconditions,such
ascavitatingneoplasm,intracavitaryclot,and
Wegenergranulomatosis[2,43,44].
Finger-in-Glove Sign
Thefingeringlovesignisthechestradio
graphicfindingoftubularandbranchingtubu
laropacitiesthatappeartoemanatefromthe
hila,saidtoresembleglovedfingers[45,46].
Thetubularopacitiesrepresentdilatedbronchi
impactedwithmucus.TheCTfingeringlove
course alongside neighboring pulmonary ar
teries. The finding is classically associated
with allergic bronchopulmonary aspergillosis
(ABPA),seeninpersonswithasthmaandpa
tients with cystic fibrosis (Fig. 15), but may
alsooccurasanimagingmanifestationofen
dobronchialtumor(Fig.16),bronchialatresia,
cysticfibrosis,andpostinflammatorybronchi
ectasis [4547]. Bronchoscopy may be nec
essarytoexcludeendobronchialtumorasthe
causeofthefingeringlovesign.
The tubular opacities that occur in ABPA
result from hyphal masses and mucoid im
pactionandtypicallyaffecttheupperlobes.In
1928%ofcases,theendobronchialopacities
inABPAmaybecalcifiedorhyperattenuating
onunenhancedCTimages(Fig.15),probably
because of the presence of calcium salts,
metals,anddesiccatedmucus[4750].
Crazy-Paving Sign
ThecrazypavingsignistheCTfindingofa
combination of groundglass opacity and
smooth interlobular septal thickening that re
semblesamasonrypatternusedinwalkways
[2].Thecrazypavingsignwasoriginallyde
scribedasacharacteristicCTpatterndetected
in patients with pulmonary alveolar pro
teinosis.Thesignhascometoberecognized,
however,asoccurringinmanyothercondi
AJR:202, March 2014 481

tions, including infection (e.g., Pneumocystis
jiroveci pneumonia, influenza, and infections
byotherorganisms)[51,52].InPneumocystis
pneumonia, the histologic features that pro
duce the crazypaving pattern are alveolar
exudates containing the infective organisms
andcellularinfiltrationoredemainthealveo
larwallsandinterlobularsepta[52,53].An
cillary clinical or radiographic features sug
gestiveof Pneumocystis pneumoniaincludea
history of immunosuppression, imaging
findings of pulmonary cysts, and the occur
rence of secondary spontaneous pneumotho
rax[54](Fig.17).
Differentialdiagnosticconsiderationsfor
the crazypaving sign can be categorized
accordingtothetypicaltimecourseofthe
suspecteddiseases(Fig.18).Diseaseschar
acterized by an acute time course include
pulmonary edema, pulmonary hemorrhage,
A and infection. Those with a more chronic
m courseincludepulmonaryalveolarproteino
eri sis, pulmonary adenocarcinoma, andlipoid
ca
pneumonia[52,55].
n
Jo
ur Grape-Skin Sign
na The grapeskin sign is the radiographic or
l
CTfindingofaverythinwalledcavitaryle
of
R sion that develops in lung parenchyma pre
oe viously affected by consolidation or lung
nt granulomas that have undergone central ca
ge
no seous necrosis [56]. As classically described,
lo the grapeskin sign is a solitary finding of a
gy thinwalledcavitywithcentrallucencythathas
20
been associated with chronic pulmonary
14
.2 coccidioidomycosis infection [57, 58] (Fig.
02 19).Overtimethelesionmaydeflate,oritmay
:4 ruptureintothepleuralspace,theresultbeing
79
pneumothorax [56, 59]. The differential
49 diagnosisofthisfindingincludesothersolitary
2. cavitaryorcysticlesions,suchasreactivation
tuberculosis infection, pneumatocele,
neoplasm (e.g., primary lung cancer or
metastasis),andotherfungalinfections.
Miliary Pattern
The miliary pattern consists of multiple
small(<3mm)pulmonarynodulesofsimilar
size that are randomly distributed throughout
bothlungs[2].Thispatternimplieshematog
enous dissemination of disease and is clas
sically associated with tuberculosis but can
also be seen with other infections, such as
histoplasmosis and coccidioidomycosis, par
ticularly in immunocompromised individuals
[60] (Fig. 20). Random pulmonary nodules
mustbedifferentiatedfromthosewithacen
trilobularorperilymphaticdistribution.Cen
Walker et al.
trilobularnodulesareevenlyspacedanddonot
come into contact with adjacent pleural
surfaces. Perilymphatic nodules are distribut
ed along peribronchovascular structures, the
subpleurallung,andalonginterlobularsepta.
Randomnodulesformingthemiliarypattern
aredistributeduniformlythroughoutthelungs,
and those in the periphery may come into
contact with a pleural surface [61, 62].
Noninfectious causes of the miliary pattern
includemetastaticdisease,IVinjectedforeign
material,andrarelysarcoidosis[62,63].
Reverse Halo and Birds Nest Signs
ThereversehalosignistheCTfindingof
peripheralconsolidationsurroundingacentral
areaofgroundglassopacity[64].Associated
irregularandintersectingareasofstrandingor
irregularlinesmaybepresentwithinthearea
ofgroundglassopacityandbecomeevidentas
thebirdsnestsign[65](Fig.21).Thesesigns
are suggestive of invasive fungal infection
(e.g., angioinvasive Aspergillus infection or
mucormycosis) in susceptible patient
populations [66]. Major predisposing factors
forfungalinfectionincludestemcellorsolid
organ transplant, hematologic malignancy,
diabeticketoacidosis,andadepressedimmune
system. Imaging features that favor
mucormycosisover Aspergillus infectionina
neutropenic patient are detection of the
reversehaloorbirdsnestsign,multiplicityof
pulmonarynodules(>10),anddevelopmentof
infection despite voriconazole prophylaxis
[6668].Thereversehaloandbirdsnestsigns
are not specific for invasive fungal infection
and may also be seen in other conditions,
includingcryptogenicorganizingpneumonia,
bacterialpneumonia,paracoccidioidomycosis,
tuberculosis, sarcoidosis, Wegener
granulomatosis,andpulmonaryinfarction[64,
6873].
Meniscus, Cumbo, and Water Lily
Signs of Echinococcal Infection
Pulmonary hydatid disease is a zoonotic
parasiticinfectioncausedbythelarvalstageof
Echinococcus tapeworms[74].Thisgenusof
wormsisendemicinAlaska,SouthAmerica,
the Mediterranean region, Africa, and
Australia.Humanscanserveasintermediate
hostsaftercontactwithadefinitivehost(e.g.,
dogorwolf)orafterconsumingcontaminated
vegetables or water [74]. The lung is the
secondmostcommonorganinvolved,afterthe
liver,andisinfectedbyeitherhematogenous
or direct transdiaphragmatic spread from the
liver[7476].
Thehydatidcystiscomposedofthreelay
ers: an outer protective barrier consisting of
modified host cells, called the pericyst; a
middle acellular laminated membrane, called
theectocyst;andaninnergerminallayerthat
produces scolices, hydatid fluid, daughter
vesicles, and daughter cysts, called the en
docyst[74,75,77].Themeniscus,Cumbo,and
waterlilysignsareallseenwithpulmonary
echinococcal infection [7478]. These signs
arecausedbyairdissectingbetweenthecyst
layers,whichareinitiallyindistinguishableon
CT images because the cysts are fluid filled
(Fig.22).Withbronchialerosion,airdissects
between the outer pericyst and ectocyst to
produce the meniscus sign (Fig. 23). Some
radiologistsbelievethatthemeniscussignis
suggestiveofimpendingcystrupture[76,77].
As it accumulates further, air penetrates the
endocyst layer and causes the Cumbo sign,
which comprises an airfluid level in the
endocyst and a meniscus sign (Fig. 23).
Finally,theendocystlayercollapsesandfloats
onfluid,formingthewaterlilysign(Fig.24).
Burrow Sign of Paragonimiasis
Paragonimiasis is a zoonotic parasitic in
fection caused by lung flukes [79]. Humans
serveasadefinitivehostwhentheyingestraw
orimproperlycookedcraborcrayfish[76].
Paragonimuswestermani and Paragonimus
kellicotti arethetwopathogensendemicto
AsiaandNorthAmerica,respectively.They
producesimilarimagingfindingsinthetho
rax[7983].
ThechestCTfindingsreflectthelifecycle
oftheparasite.Thesecondformoftheimma
tureorganismlivesinthecraborcrayfish.Af
teringestionbya mammal,theparasitepen
etrates through the small bowel to enter the
peritoneal cavity, where it incites an inflam
matory reaction. Several weeks later, the or
ganismmigratesthroughthediaphragmtoen
terthepleuralspace.Afterfindingmates,the
parasites burrow through the visceral pleura
intothelungparenchyma,wheretheyproduce
cyststhatcontaineggs.Theeggsareextruded
into bronchioles and expectorated by the
infected mammal to complete the life cycle
[79].Theburrowsignisalineartrackextend
ingfromthepleuralsurfaceorhemidiaphragm
toacavitaryorcysticpulmonarynodule.The
lineartrackrepresentsthepathfollowedbythe
worms within the lung, and the cavitary or
cystic pulmonary nodule contains both the
adultwormsandtheireggs(Fig.25).
482 AJR:202, March 2014