1273

Varied RadiologicAppearances of Pu!-monary Aspergillosis1Brad H. Thompson, MD

William Stanford, MD

Jeffrey R. Galvin, MD

Yasuyuki Kurlliara, MD

This article meets the

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Pulmonary aspergilosis represents a common, potentially lethal oppor-

tunistic infection that has four unique forms: allergic bronchopulmonaryaspergillosis (ABPA), aspergilloma, and invasive and semi-invasive asper-

gillosis. In individuals who are at risk, pulmonary aspergillosis is charac-

terized by a spectrum of clinical and radiographic findings that are in-

trinsically related to the status of the immune system or the presence of

structural lung disease. ABPA, occurring almost exclusively in asthma

patients, is characterized radiographically by fleeting pulmonary alveolar

opacities caused by deposition of immune complexes and inflammatory

cells within the lung parenchyma. Mucus plugging and bronchial wall

thickening can be expected in time. Aspergilloma, occurring in patients

with structural lung disease, typically appears radiographically as a focalintracavitary mass and is characterized initially by an increase in the wall

thickness of a preexisting cavity or cyst. Invasive aspergillosis, which oc-curs primarily in profoundly immunocompromised patients, may exhibit

nonspecffic patchy nodular opacities or lobar-type air-space disease in

cases with vascular invasion. Computed tomography may reveal a halo

or ground-glass attenuation and is more accurate in the detection of

early disease. Cavitation often develops with time and typically results inthe air crescent sign. Semi-invasive aspergillosis is radiographically simi-

lar to the invasive form but differs in clinical course, being associatedwith mild immunosuppression or chronic illness and typically progress-

ing over the course of months rather than weeks.

Abbreviations: ABPA = allergic hronchopulmonarv aspergillosis. Ig = immunoglohukn

Index terms: Aspergillosis. 60.2056. 60.634 . Lung. infection, 60.2056. 60.63-1 . Lung neoplasms. 60.319

RadloGraphics 1995; 1 5: 1 2�3- 1284

I From the Department of Radiology (B.H.T., W.S.. J.R.G.), The University of Iowa College of Medicine. 200 Hawkins I)r,

Iowa Cite. IA 52242 and the Department of Radiology. St Marianna tiniversity. Kanagawa. Japan O.K.). Presented as a sd-

efltifld exhibit at the 1994 RSNA scientifid assembly. Received February 1. 1995; revisions requested March and re-

ceivedjune 1: acceptedjune 6. Address reprint requests to B FIT.

, RSNA. 1995

Classification Scheme for Puhnonary Aspergillosis

Aspergillosis

Type Lung Structure Immune Status Pathophysiology Radiologic Features

Allergic Normal; thick Hypersensitivity Local hypersensitivity re- Central bronchiectasis,

secretions action leading to bron- mucoid impaction,

chiectasis, intermittent recurrent infiltratesbronchial plugging,

allergic pneumonia

Aspergilloma Abnormal: pre- Normal Saprophytic growth Typical fungus ball

existing cavity growing in pre-

or structural existing cavity

lung disease

(eg, sarcoid,

tuberculosis)

Invasive Normal Severely im- Vascular invasion with Early: round nodulesmunocom- thrombosis or infarc- with halo; later (2

promised tion, parenchymal wk): cavitation or

(granulocy- necrosis infarction, air cres-

topenic) cent sign

Semi-invasive Normal to mild Normal to mild Cavity formation by ftln- Slow progressive or

abnormalities immunode- gus due to chronic chronic infiltrate,

(eg, fibrosis) ficiency local growth and in- slowly developing

flammation via endo- cavity with or with-

toxins or proteolytic out air crescent sign

enzymes or aspergilloma

Figure 1. Photomicrograph (original magnifica-

tion, x200; periodic acid-Schiff stain) of the fungus

Afumigatus in its hyphal form. Note the characteris-

tic septated appearance and the dichotomous 45#{176}

branching.

1274 U Scientific Exhibit Volume 15 Number 6

U INTRODUCTIONAspergillus is a ubiquitous fungus that exists as

a saprophyte in nature and when inhaled, is Ca-

pable of causing considerable pathogenesis

within the respiratory tract in humans. Pulmo-

nary aspergillosis represents a common and po-

tentially lethal opportunistic infection that has

four distinct radiologic manifestations. Because

of the morbidity and mortality associated withpulmonary Aspergillus infections, early recogni-

tion constitutes an important task for all practic-

ing radiologists. Fortunately, each form is asso-

ciated with specific predisposing host risk

factors. In addition, each form possesses charac-

teristic radiologic features, which, when

viewed in the appropriate clinical setting,

should immediately suggest the diagnosis. Spe-

cifically, each manifestation of pulmonary as-

pergillosis depends primarily on the host’s im-

mune response to the organism. A simple classi-

fication scheme of pulmonary aspergillosis can

therefore be constructed, contingent on the in-

tegrity of the host immune system (Table).

The purpose of this article is to review in

depth the radiologic appearances and clinical

features of each form of pulmonary aspergillo-

sis, and to demonstrate how the pulmonary

manifestations occur in relation to the level of

host immunity and the presence of structural

lung disease.

U ALLERGIC BRONCHOPULMONARYASPERGILLOSIS

Allergic bronchopulmonary aspergillosis

(ABPA) represents a complex hypersensitivity

reaction to Aspergillus spores, occurring almost

exclusively in asthma patients and occasionally

as a complication of cystic fibrosis ( 1 -4). The

most common species to produce ABPA is As-

pergillusfumigatus (Fig 1). Once the organism

-� : . . � � � � � �#{149}

� -,. . .�.

November 1995 Thompson et al U RadioGraphics #{149}1275

Figure 3. ABPA in a 36-year-1d asthma patient with allergic bronchopulmonary aspergillosis. Posteroanterior

radiograph (a) demonstrates central bronchiectasis, which is better seen on the chest CT scan (b). The pres-

ence of central saccular bronchiectasis is highly suggestive of ABPA.

Figure 2. CT scan of a 33-year-old asthma patient

with ABPA shows central bronchiectasis and tubular

shadowing, which represents an area of mucoid im-

paction (*).

is deposited within the respiratory tract, an in-

tense reaction ensues with the production of

immunoglobulin (Ig) E and IgG antibodies.

Once inhaled, the organism becomes entrappedwithin inspissated mucus (mucus plugs); it

does not appear to have invasive characteris-

tics. An initial and immediate Type I hypersensi-

tivity reaction to the spores occurs, resulting

in intense bronchospasm and bronchial wall

edema due to IgE release ( 1 - 1 1 ). Immune corn-

plex deposition (IgG) elicits a subsequent in-flarnrnatory reaction that eventually leads to

bronchial wall damage, bronchiectasis, and pul-

rnonary fibrosis (1,2,4,8-11).

Clinically, patients with ABPA experience

wheezing, cough, and fever. Unfortunately,none of the clinical symptoms are specific for

ABPA, and all may be seen with cystic fibrosis,

extrinsic allergic alveolitis, recurrent pneu-

monias, or other forms of eosinophilic lung dis-

ease. Eosinophilia and elevated serum IgE levels

are typically found in ABPA, but again, they are

only suggestive ofthe diagnosis (1-3,5,6,8,12).

In approximately 20%-60% of patients, mucusplug expectoration may suggest the diagnosis

(2-4,5,6,8, 1 3). Occasional bouts of hemoptysis

may be seen in 34%-68% of cases (4).

The radiographic manifestations of ABPA arecomposed initially of fleeting pulmonary alveo-

lar opacities that represent deposition of im-

mune complexes and inflammatory cells (eosi-nophils) within the lung parenchyma (1,4,5,8,

1 1 , 1 4- 17). This is the most common radio-

graphic appearance ofABPA. With time and as

irreversible bronchial wall damage occurs, mu-

cus plugging and bronchial wall thickening can

be expected. Characteristic tubular shadows

representing mucus plugging may be transient

or remain stable for months (Fig 2). Inspissated

secretions within the central bronchi may

mimic hilar adenopathy on radiographs ( 1 1,13,

16). The presence of central saccular bronchi-

ectasis is highly suggestive of ABPA and is con-sidered the hallmark of the disease (Fig 3)

(1,2,4-6,8,9,1 1-19). These airway abnormali-

a. C.

b.

1276 #{149}Scientific Exhibit Volume 15 Number 6

Figure 4. ABPA in a 23-year-old man with asthma. Three se-

quential posteroanterior chest radiographs show progressive

postobstructive atelectasis of the right upper lobe due to cen-tral mucoid impaction. Thickening of the right upper lobe

bronchovascular bundles seen m b reflects inspissated mucus.

ties may in turn lead to areas of postobstructive

atelectasis (Fig 4) or air trapping and subse-quent pneumothorax (1 1 , 1 5, 19). Extensive

cavitation has been described as an occasional

pulmonary manifestation of ABPA (4, 1 1,12,15).

If left untreated, chronic disease may progress

to pulmonary fibrosis (14, 17, 19). Because of

the inherent risk of developing end-stage lungdisease, it is important not to overlook ABPA in

symptomatic asthmatic individuals.

Results of laboratory studies that suggest the

diagnosis of ABPA include elevated serum levelsofAspergillus-specific IgE (> 1 ,000 ng/mL[>1,000 l.tg/L]) (1-5,8-10,12-14,17). Patients

usually also have peripheral eosinophilia (1-5,

8, 1 3, 1 7). Approximately 70%-90% of patients

have precipitating IgG antibodies against As-

pergillus; thus, in those with a negative skin

test, the diagnosis of ABPA is unlikely (1-6,8-10,

12-14).Oral prednisone remains the mainstay for

treating ABPA. The efficacy of treatment can be

followed by monitoring serum levels of IgE(1,2,4,8,16) Constant surveillance with labora-

tory studies and radiographs may be necessary

in a subset of patients who become reinfected

but remain clinically asymptomatic. In these pa-tients, the redevelopment of fleeting opacities

and a concomitant rise in the level of serum IgEstrongly suggest recurrence of pulmonary as-

pergillosis (5,19).

Bronchocentric granulomatosis represents a

more localized Aspergillus infection character-ized by granulomatous inflammation of lung tis-

sue, primarily centered along and involving

bronchioles. Occurring in young asthmatic mdi-

viduals, this disease is considered a subset of

ABPA (6).

a. b.

Figure 5. Photograph of a gross surgical specimen

of a pulmonary aspergilloma (arrow) that formedwithin a left upper lobe bronchogenic cyst.

November 1995 Thompson et al #{149}RadioGrapbics #{149}1277

Figure 6. Aspergilloma in a 68-year-old woman with previous tuberculosis. Posteroanterior

(a) and lateral (b) radiographs show a 2-cm fungus ball (arrow) within a cavity in the left up-

per lobe.

N ASPERGILLOMAAspergilloma formation represents a saprophy-

tic infection in patients with preexisting struc-

tural lung disease. Patients at risk for aspergil-loma development have cavitary, bullous, or

cystic lung disease that is commonly a result of

tuberculosis, sarcoidosis, and emphysema(2,3,5-7, 1 4, 17,20). Aspergillomas have a re-

ported prevalence of 50% in association with

these diseases and are commonly encounteredas solitary lesions, primarily in the upper lobes

(2,5,7,20).

Pathologically, the fungus replicates within

an air-filled cavity creating a ball of intertwined

hyphae, mucus, and inflammatory cells (Fig 5)

(3,5,6,14,20,21). In the majority ofcases, the

aspergilloma remains clinically quiescent, often

for many years (2,5). Patients may exhibitcough, weight loss, and recurrent hemoptysis,

which occurs in 50%-80% of cases (2,3,17).

The hemoptysis results from disruption of theabundant granulation tissue that lines the pul-

monary cavity (2,7, 14). Although usually mini-

mal, it can reach life-threatening proportions,

with massive hemoptysis causing death in ap-

proximately 5% of patients (5). The overall mor-

tality rate has been reported as high as 3 1 % at 5

years, with many patients succumbing to con-

current pulmonary infections or respiratory fail-

ure (20).

At radiography, an increase in the wall thick-ness of a preexisting cavity or cyst, compared

with that seen on baseline images, suggests sec-

ondary bacterial or fungal infection (2,6, 14). An

aspergilloma appears as a focal intracavitary

mass, typically in the upper lobes, on plain ra-

diographs (Fig 6) (3,6). Measuring 3-6 centime-

ters in diameter, aspergillomas are characteristi-call)’ associated with adjacent pleural thicken-

ing (5,6,10,17). CT affords better detection ofsmaller lesions that may not be apparent on

plain radiographs. CT can also better demon-

a. b.

1278 U Scientific Exhibit Volume 15 Number 6

Figure 7. Aspergilloma in a 71-year-old man with sarcoidosis. (a) Posteroanterior radiograph shows extensive

upper lobe fibrosis. A 1 .5-cm intracavitary fungus ball (arrow) in the left upper lobe is better demonstrated on

the prone CT scan (b).

strate the relationship between the fungus andsurrounding cavity wall (Fig 7). The fungus ball

often moves with changes in patient position,but lack of movement is not uncommon (6,20).

An aspergilloma may be surrounded by a cres-

cent of air (Monod sign), thereby mimickingthe cavitation that is seen with invasive asper-gillosis (2,3,5,6, 17). This air crescent is readily

identifiable on both plain radiographs and CT

scans. Occasionally, the fungus ball may corn-

pletely fill the cavity, and no air crescent will

be present (20).

Treatment options vary and are primarily

dictated by the clinical status of the patient.Asymptomatic patients may require only peri-

odic radiologic surveillance. Spontaneous reso-

lution of aspergillomas is uncommon, occurring

in only 10% of cases (2,6, 1 0, 1 4). Because of the

inherent risk of life-threatening hemoptysis,

many patients require some form of medical

intervention. Treatment options are primarily

limited to either systemic antifungal therapy or

surgical removal of the cavity. Systemically ad-ministered amphotericin B has often been mini-

mally effective because of poor delivery to the

center of the cavity, and it poses a substantial

risk of nephrotoxicity and liver injury (22). Al-

though surgical resection of an aspergilloma is

curative in 85%- 100% of patients, many mdi-viduals are not surgical candidates due to their

underlying lung disease (2,3,6,20). Intracavitary

infusion of antiftlngal agents has been reported

to be a successful treatment alternative

�#

“SFigure 8. Acute Aspergillus infection. CT image of

a bone marrow transplant patient shows an area ofair-space disease in the right upper lobe. Bronchos-

CO�� revealed Aspergillus nodules.

(6,22,23). Embolization of feeding vessels(bronchial or intercostal arteries) with polyvi-

nyl alcohol particles represents another treat-

ment option for patients with hemoptysis. Al-

though embolization can be an effective means

for controlling bleeding, the results may not be

definitive; 20% of patients will experience re-

current bouts of hemoptysis (22).

U INVASiVE ASPERGILLOSISInvasive pulmonary aspergillosis is a potentially

lethal opportunistic infection that primarily oc-

curs in patients who are profoundly immuno-

compromised, such as individuals who have re-

cently undergone bone marrow transplantation

or patients with hematologic malignancies, es-

pecially leukemia. Invasive aspergillosis has also

been encountered in patients with chronic ob-structive pulmonary disease and others who arenot immunocompromised (3,24,25). Familiarity

#{176}�. -�

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.‘ 4’

j�: � ;..�

a. b.

November 1995 Thompson et al U RadioGraphics #{149}1279

Figure 9. Invasive aspergillosis in a 38-year-old woman with acute myclogenous leukemia who had undergone

bone marrow transplantation. Posteroanterior radiograph (a) shows a large, ill-defined Aspergillus nodule in the

left upper lobe, which on the CT scan (b) has a characteristic “halo sign (representing hemorrhage).

with the radiologic manifestations of this form

of aspergillosis is critical, for without early de-

tection and appropriate treatment, invasive as-pergillosis carries a mortality rate approaching

65-90% (7,24-28).

Aspergilus organisms exist as airborne

spores that can be inhaled and deposited within

the respiratory tract. In individuals with normal

immunity, the spores are phagocytized and im-

mediately killed by macrophages. Added pro-

tection is provided by neutrophils and mono-

cytes, which together are capable of killing

spores and developing hyphae. If abnormalities

exist in these defense mechanisms, the As-

pergilus spores undergo germination and turn

into invasive hyphae (Fig 1) (5,6). The extent

and severity of infection in susceptible individu-

als are of course predicated on the degree of

immunodeficiency; individuals with profound

granulocytopenia and those with defective

mononuclear phagocytic function are at risk

(3,5). Obviously, patients with both defects are

at greatest risk. The following diseases and con-ditions place individuals at an increased risk for

secondary invasive pulmonary aspergillosis: leu-

kemia and hematologic malignancies, bone mar-

row transplantation, high-dose corticosteroid

therapy, Cushing syndrome, aplastic anemia,

and chronic granulomatous disease of child-

hood. The aggregate risk is related to the dura-

tion of neutropenia. Individuals with normal

immunity can develop invasive aspergillosis;

known as primary invasive pulmonary aspergil-

losis, this form occurs in patients who have re-

ceived a tremendous inoculation of spores

(3,6).

The lung is the only site of infection in 60%

ofpatients with invasive aspergillosis (3,5,14).

Additional sites of infection include the brain,

liver, kidney, and gastrointestinal tract and oc-

cur in approximately 1 5%-30% of individuals

(3,5,6, 14,25). Clinically, patients present with

fever, nonproductive cough, and occasional

chest pain. In patients with profound neutro-

penia, the febrile response may be minimal. Be-

cause of the aggressive characteristics of the

fungus, vascular invasion of small vessels oc-

curs; this may result in hemoptysis and may he

life-threatening.

Secondary invasive pulmonary aspergillosisoccurs approximately 25 days after the initia-

tion of chemotherapy or the induction of hone

marrow aplasia (5,6,26,27,29). The greatest risk

occurs when the white blood cell count is less

than 500 mm3(0.5 x 10� cellsfL) (5,6,26,27,29).

Lesions caused by Aspergillus organisms start

with endobronchial proliferation followed by

transbronchial vascular invasion, eventually

causing thrombosis and infarction of lung tissue

(3,7,14,17,25,27,30,31). Early in the infection,

plain radiographs or CT scans may exhibit non-

specific patchy nodular opacities or lobar-type

air-space disease that characterize the angioin-vasive form of aspergillosis (Fig 8) (3,27,28,31).

On CT scans, Aspergillus nodules tend to have

a characteristic halo of ground-glass attenuation

that represents areas of pulmonary hemorrhage

(Fig 9) (6,7, 1 7,26,27,3 1 ,32). Although nodules

with halos have been described in many dis-

a. b.

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1280 #{149}Scientific Exhibit Volume 15 Number 6

Figure 10. Invasive aspergillosis in a 3 1-year-old man with acute myelogenous leukemia who had undergone

hone marrow transplantation. (a) Posteroanterior radiograph shows a subtle nodule in the left upper lobe (ar-

row). (b) CT scan obtained the next day shows several Aspergillus nodules that were not readily apparent on

the plain radiograph.

eases (33), in the appropriate clinical setting,the CT demonstration of the halo sign is consid-

ered very specific ( 100%) for invasive aspergil-

losis (28).

Occasionally, invasive aspergillosis may ap-

pear as peribronchial opacities (27) or as focal

areas of pneumonic consolidation, which are

manifestations of an Aspergillus infection

known as invasive aspergillosis of the airways

(ulcerative tracheobronchitis) (6, 14,30). Re-

flecting a primary infection of the tracheobron-

chial tree, this form is less common than the

angioinvasive type, constituting approximately

lO%-34% of cases (2, 1 4,30). Invasive aspergillo-

sis of the airways can exist alone, without coex-

isting vascular invasion, and has a mortality rate

equal to that of the angioinvasive form (30).Early in the disease, Aspergillus nodules may

be small and not readily apparent on plain ra-

diographs. Because approximately 30% of pa-

tients with proved pulmonary aspergillosis have

normal results at chest radiography, further in-

vestigation with CT is recommended in febrile

patients at risk for aspergillosis (10,14,32).

Studies have shown CT to have higher sensitiv-

ity (27) and specificity (28) than radiography in

the detection of early disease. CT is clearly ad-

vantageous for the surveillance of early aspergil-

losis and permits detection and better charac-

terization of small fungal nodules at a time

when the initiation of antifungal therapy has

Figure 11. Invasive aspergillosis. Photomicro-

graph (original magnification, x20; hematoxylin-

eosin stain) shows fungal invasion of a pulmonary ar-

teriole with thrombosis of the lumen.

the greatest likelihood of success (Fig 10) (31).

CT may also reveal unsuspected sites of infec-

tion in the liver or spleen. By permitting accu-

rate localization of sites of infection, CT also is

useful in directing percutaneous needle biopsyor bronchoscopy, thereby maximizing the diag-

nostic success of lavage or biopsy. In general,

the CT appearance of invasive aspergillosis is so

characteristic that additional confirmatory diag-

nostic tests such as bronchoscopy may not be

required. At our institution, amphotericin B

treatment is initiated in almost all neutropenic

patients who have pulmonary nodules charac-

a. b.

C. d.

November 1995 Thompson Ct al U RadioGraphics #{149}1281

Figure 12. Invasive aspergillosis in a 33-year-old female bone marrow transplant recipient. (a, b) Posteroante-nor radiograph (a) and CT scan (b), both obtained in I)ecember 1993, show an Aspergillus nodule in the leftupper lobe. (c, d) Posteroanterior radiograph (c) and CT scan (d) obtained 4 weeks later show cavitation of the

nodule. The circumferential collection of air around the nodule is known as the air crescent sign.

teristic of invasive aspergillosis. CT then serves

an important role in monitoring the efficacy of

treatment.

With time, approximately 45%-50% of the

fungal nodules will undergo cavitation (6,29).

The process of cavitation relies primarily on an

increased granulocytic response and therefore

coincides with bone marrow recovery. It is also

related in part to coincidental pulmonary infarc-

tion that arises as a result of vascular invasion

(thrombosis) (Fig 1 1). Cavitation typically oc-

curs 6-26 days (mean, 1 5 days) after the onset

of infection when the white blood cell count

exceeds 1,000/mm3 (1.0 x l0� cells/L) (6,27,29,

31).

The process of cavitation characteristically

results in the air crescent sign, which histologi-

cally represents necrotic lung intermixed with

hyphae, surrounded by a thin rim of air (cavity)

(Fig 12) (10,14,17,21,31,34). At this stage, the

radiographic appearance of the air crescent her-

aIds the recovery phase of invasive aspergillosis

(6,26,29,32). It is uncommon for invasive asper-

gillosis to progress once the cavitary phase oc-

curs (29). Patients in whom the fungal nodules

do not cavitate despite bone marrow recovery

a. b.

1282 U Scientific Exhibit Volume 15 Number 6

Figure 13. Semi-invasive aspergillosis in a 30-year-old diabetic woman. (a) Posteroanterior radio-graph (October 1974) shows a small fungal nodule in the upper lobe (arrow) that proved to be As-

pergillus at bronchoscopy. (b) Posteroanterior radiograph obtained in 1 983 shows subsequent cavita-

tion and enlargement of the fungal infection. Patient remained asymptomatic and received flO treat-

ment in the interval between the two radiographs. This case shows the typically prolonged clinicalcourse of semi-invasive aspergillosis.

tend to have a poorer prognosis and a higher

mortality (29). This may in part reflect a persis-

tent qualitative defect in granulocytic function.

Like the halo sign, in the appropriate clinical

setting, the air crescent sign is very suggestive

of invasive aspergillosis. However, because

cavitation occurs late in the course of the infec-tion, recognition and diagnosis of invasive as-

pergillosis at this stage mean treatment has

been substantially delayed. Also, although inva-

sive aspergillosis is the most common cause of

the air crescent sign, the sign may be seen in

other diseases, such as tuberculosis, actinomy-

cosis, bacterial abscess, mucormycosis, septic

emboli, and carcinoma (5,6, 18,29,34). Because

radiographic similarities exist, care must betaken not to confuse the air crescent sign of in-

vasive aspergillosis with Monod sign of aspergil-

loma (2 1,35).

U SEMI-INVASiVE ASPERGILLOSIS

The semi-invasive form of aspergillosis is very

similar radiographically to its more invasive

counterpart, differing primarily in the clinical

course. Characteristically, patients susceptible

to semi-invasive aspergillosis are mildly immu-

nocompromised or have chronic illnesses that

predispose them to infection (2,6, 17). The typi-

cal time course of the semi-invasive form cx-

tends over a period of months, not weeks as in

invasive aspergillosis, with the rate of progres-

sion dependent on the degree of immunosup-

pression (2,6,36). Furthermore, the presence of

superimposed structural lung disease adds an

additional risk factor for infection. Risk factors

for semi-invasive pulmonary aspergillosis in-

dude diabetes mellitus, alcoholism, pneumo-

coniosis, collagen vascular disorders, chronic

obstructive pulmonary disease, previous radia-

tion therapy, malnutrition, myocardial infarc-

tion, and low-dose steroid use.

Initial fungal colonization of the lungs is

similar to that seen with invasive aspergillosis,

but the onset of cavitation occurs 5-7 months

after the start of the infection. During this pe-

riod, the patient typically complains of cough

and may have leukocytosis, sputum production,

and fever. Pathologically, the fungus behavessimilarly to the more invasive form, with even-

tual vascular invasion, suppuration, and cavita-

tion (Fig 1 3). Like patients with the invasiveform, patients with semi-invasive aspergillosis

may experience recurrent bouts of hemoptysis.

November 1995 Thompson et al #{149}RadioGrapbics #{149}1283

Radiographically, semi-invasive aspergillosis

commonly appears as a chronic upper lobe

opacity, thereby mimicking a mycobacterial in-

fection (6). As is true with invasive aspergillo-

sis, cavity formation is a manifestation of the

invasiveness of the fungus and does not reflect

inhabitation of a preexisting cavity. Isolation of

the fungus with repeated sputum cultures can

help confirm the diagnosis (6).

Treatment options depend primarily on the

status of the patient; observation may be all that

is required in asymptomatic patients. Antifungal

agents (amphotericin B or itraconazole) are

common treatments that can be administered

either systemically or directly into the lesion in

a manner similar to that described for the treat-

ment of aspergillomas. In patients with hemop-tysis, surgical resection of the lesion provides a

more definitive therapeutic alternative (6).

U CONCLUSIONSThis article is intended to give the reader a

greater appreciation of the spectrum of pulmo-

nary aspergillosis and its concurrent radiologic

manifestations. Pulmonary aspergillosis repre-

sents a relatively common and potentially fatal

infection, especially in severely immunocom-

promised patients. For this reason, a high level

of suspicion and a thorough knowledge of the

forms of aspergillosis are necessary for all prac-

ticing radiologists. The forms of pulmonary as-

pergillosis should not necessarily be compart-

mentalized into discrete entities; pulmonary as-

pergillosis represents a continuum of disease,

the manifestations of which are contingent on

host immune response and the structural integ-

rity of the lung.

U REFERENCES1 . Greenherger PA. Allergic bronchopulmonary

aspergillosis and fungoses. Clin Chest Med

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This article meets the criteriafor 1.0 credit hour in Category 1 of the AMA Phsician ‘s Recognition

Award. To obtain credit, see the questionnaire on pp 1499-1502.

1284 U Scientific Exhibit Volume 15 Number 6

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