Allergic bronchopulmonary aspergillosis - CHEST Publications ...

CHEST Global Medicine 

Allergic Bronchopulmonary 

Aspergillosis* 

Ritesh Agarwal, MD, DM, FCCP 

Allergic bronchopulmonary aspergillosis (ABPA) is an immunologic pulmonary disorder caused 

by hypersensitivity to Aspergillus fumigatus. Clinically, a patient presents with chronic asthma, 

recurrent pulmonary infiltrates, and bronchiectasis. The population prevalence of ABPA is not 

clearly known, but the prevalence in asthma clinics is reported to be around 13%. The disorder 

needs to be detected before bronchiectasis has developed because the occurrence of bronchiectasis 

is associated with poorer outcomes. Because many patients with ABPA may be minimally 

symptomatic or asymptomatic, a high index of suspicion for ABPA should be maintained while 

managing any patient with bronchial asthma whatever the severity or the level of control. This 

underscores the need for routine screening of all patients with asthma with an Aspergillus skin 

test. Finally, there is a need to update and revise the criteria for the diagnosis of ABPA. This 

review summarizes the advances in the diagnosis and management of ABPA using a systematic 

search methodology. (CHEST 2009; 135:805–826) 

Key words: allergic bronchopulmonary aspergillosis; Aspergillus; bronchial asthma; cystic fibrosis; prevalence 

Abbreviations: AAS allergic Aspergillus sinusitis; ABPA allergic bronchopulmonary aspergillosis; ABPA-CB allergic 

bronchopulmonary aspergillosus with central bronchiectasis; ABPA-CB-ORF allergic bronchopulmonary aspergillosus with 

central bronchiectasis and other radiological findings; ABPA-S seropositive allergic bronchopulmonary aspergillosus; 

AH Aspergillus hypersensitivity; CF cystic fibrosis; HRCT high-resolution CT; IL interleukin 

Aspergillus is a ubiquitous mold representing between 

0.1% and 22% of the total air spores 

sampled. 1 There are approximately 250 species of 

Aspergillus, but only a few are human pathogens. 2,3 

Depending on the host immunity and the organism 

virulence, the respiratory diseases caused by Aspergillus 

are classified as saprophytic (aspergilloma), 

allergic (allergic Aspergillus sinusitis, allergic bronchopulmonary 

aspergillosis [ABPA], and hypersensitivity 

pneumonias) and invasive (airway invasive aspergillosis, 

chronic necrotizing pulmonary aspergillosis, and 

invasive aspergillosis). 4 ABPA is an allergic pulmonary 

disorder caused by hypersensitivity to Aspergillus fu- 

*From the Department of Pulmonary Medicine, Postgraduate 

Institute of Medical Education and Research, Chandigarh, India. 

The author has no conflicts of interest to disclose. 

Manuscript submitted November 4, 2008; revision accepted 

November 20, 2008. 

Reproduction of this article is prohibited without written permission 

from the American College of Chest Physicians (www.chestjournal. 

org/misc/reprints.shtml). 

Correspondence to: Ritesh Agarwal, MD, DM, FCCP, Assistant 

Professor, Department of Pulmonary Medicine, Postgraduate 

Institute of Medical Education and Research, Sector-12, Chandigarh 

160012, India; e-mail: riteshpgi@gmail.com 

DOI: 10.1378/chest.08-2586 

migatus clinically manifesting as chronic asthma, recurrent 

pulmonary infiltrates, and bronchiectasis. 5–13 The 

condition has immunologic features of immediate hypersensitivity 

(type I), antigen-antibody complexes 

(type III), and eosinophil-rich inflammatory cell 

responses (type IVb), based on the revised Gell and 

Coombs classification of immunologic hypersensitivity. 

14,15 The disorder was first described by Hinson et 

al 16 in 1952 in the United Kingdom. Occasionally, 

patients can develop a syndrome similar to ABPA, 

but it is caused by fungi other than A fumigatus and 

is called allergic bronchopulmonary mycosis. 17 The 

prevalence of ABPA is believed to be about 1 to 2% 

in patients with asthma and 2 to 15% in patients with 

cystic fibrosis (CF). 13 The condition remains underdiagnosed 

in many countries with reports of mean diagnostic 

latency of even 10 years between the occurrence 

of symptoms and the diagnosis. 18 In the past two 

decades, there has been an increase in the number 

of cases of ABPA due to the heightened physician 

awareness and the widespread availability of serologic 

assays. 19–23 This review provides a summary of 

the advances in the field of ABPA. For the purpose of 

this review, a systematic search of PubMed and Em- 

www.chestjournal.org CHEST / 135 /3/MARCH, 2009 805 

Downloaded From: http://jupcvss.chestpubs.org/ on 08/01/2013

Table 1—Studies Describing the Prevalence of AH and/or ABPA in Patients with Bronchial Asthma Over the Last 

Two Decades* 

Study/Year Type of Study 

Type of Skin 

Test Type of Antigen 

Attapattu 31 /1991 Prospective Intradermal Commercial (Bencard 

Allergie; Munich, 

Germany) 

Eaton et al 33 /2000 

Kumar and Gaur 

Prospective Prick Commercial (Hollister- 

Stier Laboratories) 

34 / 

2000 

Base was performed for relevant studies published from 

1952 to 2008. A total of 250 articles were reviewed for the 

purpose of this article. 

Epidemiology of ABPA 

Aspergillus hypersensitivity (AH) is defined by the 

presence of an immediate-type cutaneous hypersensitivity 

to A fumigatus antigens, and it is the first step 

in the development of ABPA. 24 Only a minority of 

patients with AH develop the complete clinical 

picture of ABPA. 25 The population prevalence of 

ABPA in asthma, generally referred to as 1 to 

2%, 5,13,26,27 is based on the inference of only three 

studies (one peer-reviewed and two non–peer-reviewed 

studies). 28,29 In the only peer-reviewed 

study, 28 14 patients with allergic bronchopulmonary 

mycosis were identified from a total of 1,390 new 

referrals in a catchment area population of half a 

million, estimating a period prevalence of just above 

1%. The other two non–peer-reviewed questionnaire-based 

studies suggested a maximum prevalence 

of ABPA of 1% in the United States. 29 In a 

recent metaanalysis, 30 we demonstrated a prevalence 

of AH and ABPA in asthma of 28% and 12.9%, 

respectively. The limitation noted in this review was 

that all the studies were performed in specialized 

clinics and may not be representative of the general 

population. Thus the exact population prevalence of 

ABPA remains speculative but is likely to be fairly 

Criteria Used for 

Diagnosis of ABPA 

Major (A/R/T/E/P) 

Minor (C) 

Prevalence of AH 

in Asthma (n/N) 

Prevalence of ABPA 

in Asthma (n/N) 

58/134 8/134 

Major (A/R/T/E/P/ 

I/C/S) 

47/255 9/35 

Prospective Intradermal Locally prepared Major (A/R/T/E/P/ 

I/C/S) 

Minor (C/S/B) 

47/200 32/200 

Al-Mobeireek et al 20 / Prospective Prick Commercial (Soluprick; 

12/53 

2001 

ALK Laboratories; 

Wallingford, CT) 

Maurya et al 35 /2005 Prospective Intradermal Locally prepared Major (A/R/T/E/P/ 

I/C/S) 

Minor (C/S) 

30/105 8/105 

Agarwal et al 23 /2007 Prospective Intradermal Commercial (Hollister- Major (A/R/T/E/P/ 291/755 155/755 

Stier Laboratories) I/C/S) 

Minor (S/B) 

Prasad et al 36 /2008 Prospective Intradermal Not available Major (A/R/T/E/P/ 

I/C/S) 

Minor (C/S/B) 

74/244 18/244 

* Criteria for ABPA: Major (A asthma, R radiologic opacities, T immediate positive skin test, E eosinophilia, P precipitins to A 

fumigatus, I IgE elevated, C central bronchiectasis, S specific IgG/IgE to A fumigatus); Minor (C sputum cultures of A fumigatus, 

S type III skin test positivity, B brownish black mucus plugs). 

high in patients attending asthma clinics. Table 1 

summarizes the prevalence of ABPA in patients with 

asthma reported in various studies 20,23,31–36 over the 

last two decades. The prevalence of ABPA in patients 

admitted with acute severe asthma is even 

higher. In a recent study of 57 patients with acute 

severe asthma admitted in the respiratory ICUs, we 

demonstrated the prevalence of AH and ABPA to be 

around 51% and 39%, respectively. 37 The occurrence 

of AH and ABPA was significantly higher in patients 

with acute asthma compared to the outpatient bronchial 

asthma (around 39% and 21%, respectively). 23 

Pathogenesis of ABPA 

The susceptibility of asthmatic patients to develop 

ABPA is not fully understood (Fig 1). Some authors 

have reported that exposure to large concentrations 

of spores of A fumigatus may cause ABPA. 16,38–41 

Environmental factors are not considered the main 

pathogenetic factors because not all asthmatics develop 

ABPA despite being exposed to the same 

environment. In a genetically predisposed individual42–54 

(Table 2), inhaled conidia of A fumigatus 

persist and germinate into hyphae with release of 

antigens that compromise the mucociliary clearance, 

stimulate and breach the airway epithelial barrier, 

and activate the innate immunity of the lung. 55–58 

This leads to inflammatory cell influx and a resultant 

early- and late-phase inflammatory reaction. 59,60 The 

806 Global Medicine 


Figure 1. A line diagram depicting the pathogenesis of allergic bronchopulmonary aspergillosis. Th T-helper. 

antigens are also processed presented to T-cells with 

activation of Th2 CD4 T-cell responses. 42,61–63 The Th2 

cytokines (interleukin [IL]-4, IL-5, and IL-13) lead to total 

and A fumigatus-specific IgE synthesis, mast cell degranulation, 

and promotion of a strong eosinophilic response. 

This causes the characteristic pathology of ABPA. 

Pathology of ABPA 

The pathology of ABPA varies from patient to 

patient, and in different areas of the lung in the same 

patient (Fig 2). 64,65 Histologic examination reveals 

the presence of mucus, fibrin, Curschmann spirals, 

Charcot-Leyden crystals, and inflammatory cells. 

Scanty hyphae can often be demonstrated in the 

bronchiectatic cavities. The bronchial wall in ABPA 

is usually infiltrated by inflammatory cells, primarily 

the eosinophils. 65 The peribronchial parenchyma 

shows an inflammatory response with conspicuous 

eosinophilia. Occasionally, fungal growth in the lung 

parenchyma can occur in some patients with ABPA. 66 

Patients can also demonstrate a pattern similar to that 

of bronchiolitis obliterans with organizing pneumonia. 

67 Bronchocentric granulomatosis, the presence of 

noncaseating granulomas containing eosinophils and 



Table 2—Genetic Factors Involved in the Pathogenesis 

of ABPA* 

HLA associations: presence of HLA DR-2 and absence of 

HLA-DQ2 sequences 42,44,45 

IL-10 promoter polymorphisms 49 

Polymorphism at position 1,082 produces higher levels of IL-10 

if 1082G allele is present and lower levels of IL-10 if the 

1082A allele is present 

In patients with CF there is a relationship between the 1082GG 

genotype with both Aspergillus colonization and ABPA 

Surfactant protein A gene polymorphisms 48,53 

A significantly higher frequency of the AGA allele (A1660G) of 

SP-A2 found in patients with ABPA vs control subjects. 

Coexistence of A1660G polymorphism with SP-A2 G1649C 

(Ala91Pro) found with 10-fold higher odds in patients with 

ABPA. Patients with ABPA with GCT and AGG alleles 

showed significantly higher levels of total IgE and percentage 

eosinophilia vs patients with ABPA with CCT and AGA 

alleles 48 

The T allele at T1492C and G allele at G1649C of SP-A2 

observed at higher frequencies in ABPA patients than in 

controls. Also there is a higher frequency of the TT genotype 

at position1492 of SP-A2 than controls 53 

There were no polymorphisms found in SP-A1 gene 53 

CFTR gene mutation: 43,46,47 increased frequency of CFTR 

mutations in patients with ABPA vs skin-prick test positive or 

negative patients with bronchial asthma 

IL-15 polymorphisms: 52 higher frequency of IL-15 13689*A 

allele and A/A genotype 

TNF- polymorphisms: 52 lower frequency of the TNF- 308 * A/A 

genotype 

Mannose-binding lectins: 53 the intronic single nucleotide 

polymorphism G1011A of mannose-binding lection seen with 

increased frequency in patients with ABPA 

IL-4 receptor polymorphisms: 51 single nucleotide polymorphism of 

the extracellular IL-4R ile75val observed in 80% of ABPA 

patients 

IL-13 polymorphisms: 50 the arg110gln polymorphism found with 

increased frequency in ABPA and the combination of IL-4R 

ile75val/IL-13 arg110gln polymorphism found with an even 

higher frequency 

Toll-like receptor gene polymorphisms: 54 susceptibility to ABPA 

was associated with allele C on T1237C (TLR9) 

*HLA human leukocyte antigen; TNF tumor necrosis factor; 

CFTR CF transmembrane conductance regulator. 

multinucleated giant cells centered on the airway, are 

also seen. 68,69 Rarely, invasive aspergillosis complicating 

the course of ABPA has also been described. 70–74 

Clinical Features 

There is no gender predilection and majority of the 

cases present in the third to fourth decade. A family 

history of ABPA may be elicited occasionally. 75 Table 3 

summarizes the clinical features of ABPA encountered 

in three large series from our institute. 19,21,23 

Most present with low-grade fever, wheezing, bronchial 

hyperreactivity, hemoptysis, or productive 

cough. Expectoration of brownish black mucus plugs 

is seen in 31 to 69% of patients. 21,23,34 The symptoms 

of hemoptysis, expectoration of brownish black mucus 

plugs, and history of pulmonary opacities in an 

asthmatic patient suggests ABPA. Patients can occasionally 

be asymptomatic, and the disorder is 

diagnosed on routine screening of asthmatic patients. 

22,23,33 Physical examination can be normal or 

may reveal polyphonic wheeze. Clubbing is rare, 

seen in only 16% of patients. On auscultation, coarse 

crackles can be heard in 15% of patients. 23 Physical 

examination can also detect complications such as 

pulmonary hypertension and/or respiratory failure. 76 

During exacerbations of ABPA, localized findings of 

consolidation and atelectasis can occur that needs to 

be differentiated from other conditions. 

Laboratory Findings 

Aspergillus Skin Test: The Aspergillus skin test is 

performed using an A fumigatus antigen, either 

commercial (eg, Aspergillin; Hollister-Stier Laboratories; 

Spokane, WA) or locally prepared. The test is 

read every 15 min for 1 h, and then after 6 to 8 h. 

The reactions are classified as type I if a wheal and 

erythema developed within 1 min, reaches a maximum 

after 10 to 20 min, and resolves within 1 to 2 h. 

A type III reaction is read after 6 h, and any amount 

of subcutaneous edema is considered a positive 

result. An immediate cutaneous hypersensitivity to A 

fumigatus antigens is a characteristic finding of 

ABPA and represents the presence A fumigatusspecific 

IgE antibodies, whereas a type III skin 

reaction probably represents the immune complex 

hypersensitivity reaction, although its exact significance 

remains unclear. The test can be performed 

using either a skin-prick test or intradermal injection 

with the latter being more sensitive. 30,77,78 A skinprick 

test should be performed for Aspergillus skin 

testing, and if the results are negative should be 

confirmed by an intradermal test. 30 There is no 

difference on the outcome of the test and the type of 

antigen (locally prepared or commercial) used for 

performance of the test. 30 

Total Serum IgE Levels: The total IgE level is the 

most useful test for diagnosis and follow-up of ABPA. A 

normal serum IgE level excludes ABPA as the cause of 

the patient’s current symptoms. The only situation 

where IgE levels can be normal in active ABPA is when 

the patient is already on glucocorticoid therapy for any 

reason and investigation for IgE levels has been conducted. 

After treatment with glucocorticoids, the serum 

IgE levels decline, and a 35 to 50% decrease is 

taken as a criteria for remission. 79 The serum IgE 

determination is also used for follow-up, and a doubling 

of the patient’s baseline IgE levels indicates relapse of 

ABPA. 80,81 



Figure 2. Histopathologic findings in a patient with allergic bronchopulmonary aspergillosis. Top left, A: 

photomicrograph showing bronchial lumen containing allergic mucin (hematoxylin-eosin, original 100). Top 

right, B: high-magnification photomicrograph of allergic mucin having variegated appearance, necrotic eosinophils, 

Charcot-Leyden crystals (thin arrow), and an occasional septate fungal hyphae indicated by a thick arrow 

(hematoxylin-eosin, original 200). Bottom left, C: photomicrograph showing eosinophilic pneumonia. There is 

filling of the alveolar spaces by eosinophils admixed with variable number of macrophages (hematoxylin-eosin, 

original 200). Bottom right, D: photomicrograph showing bronchocentric granulomatosis. There is partial 

replacement of bronchial epithelium by palisading histiocytes (hematoxylin-eosin, original 100). 

Serum IgE and IgG Antibodies Specific to A 

fumigatus: An elevated level of A fumigatus-specific 

antibodies measured by fluorescent enzyme immunoassay 

is considered the hallmark of ABPA. 22 A 

cutoff value of IgG/IgE more than twice the pooled 

serum samples from patients with AH can greatly 

help in the differentiation of ABPA from other 

conditions. 82 

Table 3—Clinical Features Encountered in Three Large Case Series of ABPA Published From the Author’s 

Institute* 

Clinical Features Behera et al 19 /1994 Chakrabarti et al 21 /2002 Agarwal et al 23 /2007 

Patients, No. 35 89 155 

Male/female gender, No. 14/21 53/35 79/76 

Mean age, yr 34.3 36.4 33.4 

Mean duration of asthma, yr 11.1 12.1 8.9 

History of asthma 94% 90% 100% 

Expectoration of sputum plugs Not available 69% 46.5% 

Mean eosinophil count, per L 1,264 

AEC 500/L, % 12/28 (43%) 100% 76.1% 

Fleeting shadows 77% 74% 40% 

History of intake of antituberculous drugs 

Skin test against Aspergillus 

34% 29% 44.5% 

Type I 51% 85% 100% 

Type III 25.7% 16.9% 83.2% 

Mean IgE levels Not done Not done 6,434 

Elevated IgE levels, % 100% 

Aspergillus-specific IgE/IgG Not done Not done 100% 

Serum precipitins against Aspergillus 77% 71.9% 86.5% 

Central bronchiectasis 

*AEC absolute blood eosinophil count. 

71% 69% 76.1% 



Radiologic Investigations: A wide spectrum of 

radiographic appearances can occur in ABPA (Table 

4). The chest radiographic findings of ABPA include 

transient or fixed pulmonary opacities (Fig 3), tramline 

shadows, finger-in-glove opacities, and toothpaste 

shadows. 83–87 Findings noted on high-resolution 

CT (HRCT) include central bronchiectasis, mucoid 

impaction, mosaic attenuation, presence of centrilobular 

nodules, and tree-in-bud opacities (Fig 

4). 88,89 High-attenuation mucoid impaction (mucus 

visually denser than the paraspinal muscle) is a 

pathognomonic finding encountered in patients with 

ABPA. 23,90–95 Central bronchiectasis with peripheral 

tapering of bronchi on HRCT is believed to be a sine 

qua non for the diagnosis of ABPA. Bronchiectasis 

may not be present in all patients with ABPA, may be 

present in patients with CF without ABPA, and 

almost 40% of the bronchiectatic segments can also 

Table 4—Radiologic Findings Encountered in Patients 

With ABPA 

1. Chest radiographic findings 

Transient changes 

Common 

Patchy areas of consolidation 

Radiologic infiltrates: toothpaste and gloved finger shadows 

due to mucoid impaction in dilated bronchi 

Collapse: lobar or segmental 

Uncommon 

Bronchial wall thickening: tramline shadows 

Air-fluid levels from dilated central bronchi filled with fluid 

Perihilar infiltrates simulating adenopathy 

Massive consolidation: unilateral or bilateral 

Small nodules 

Pleural effusions 

Permanent changes 

Common 

Parallel-line shadows representing bronchial widening 

Ring-shadows 1–2 cm in diameter representing dilated 

bronchi en face 

Pulmonary fibrosis: fibrotic scarred upper lobes with 

cavitation 

Uncommon 

Pleural thickening 

Mycetoma formation 

Linear scars 

2. HRCT findings 

Common 


Mucus plugging with bronchoceles 

Consolidation 

Centrilobular nodules with tree-in-bud opacities 

Bronchial wall thickening 

Areas of atelectasis 

Mosaic perfusion with air trapping on expiration 

Uncommon 

High-attenuation mucus (finding most helpful in differential 

diagnosis) 

Pleural involvement 

Randomly scattered nodular opacities 

have associated peripheral bronchiectasis. 22,96 Minimal 

bronchiectasis can also be seen in asthma, 97,98 

but the findings of bronchiectasis affecting three or 

more lobes, centrilobular nodules, and mucoid impaction 

are highly suggestive of ABPA. 99 The uncommon 

radiologic manifestations of ABPA include 

miliary nodular opacities, 100 perihilar opacities 

simulating hilar lymphadenopathy, 84,101,102 pleural 

effusions, 103–105 and pulmonary masses. 106–111 

Serum Precipitins Against A fumigatus: The precipitating 

IgG antibodies are elicited from crude 

extracts of A fumigatus and can be demonstrated 

using the double gel diffusion technique. 112,113 They 

can also be present in other pulmonary disorders and 

thus represent supportive not diagnostic evidence for 

ABPA. 112–114 

Peripheral Eosinophilia: A blood absolute eosinophil 

count 1,000 cells/L is also a major criterion 

for the diagnosis of ABPA. However, 53% of patients 

in our series 22 had an absolute eosinophil count 

1,000 cells/L, and thus a low eosinophil count 

does not exclude the diagnosis of ABPA. 

Sputum Cultures for A fumigatus: Culture of A 

fumigatus in the sputum is supportive but not diagnostic 

of ABPA. The fungus can also be grown in 

patients with other pulmonary diseases due to the 

ubiquitous nature of the fungi. We rarely perform 

sputum cultures for the diagnosis of ABPA. 

Pulmonary Function Tests: These tests help categorize 

the severity of the lung disease but have no 

diagnostic value in ABPA and need not constitute 

the basis for screening. 22 The usual finding is an 

obstructive defect of varying severity. 115–117 

Role of Specific Aspergillus Antigens: Patients with 

ABPA are evaluated with crude extracts from Aspergillus, 

which lack reproducibility and consistency, 

and they frequently cross-react with other antigens. 

118 The advances in molecular techniques have 

enabled detection and cloning of specific Aspergillus 

antigens. The recombinant allergens Asp f1, Asp f2, 

Asp f3, Asp f4, and Asp f6 have been evaluated for 

their diagnostic performance in serologic studies in 

asthmatic patients 119–122 and in patients with 

CF 121,123–125 Preliminary data suggest a promising 

role of these antigens in the diagnosis of ABPA. 

Further studies are required before they can be 

implemented in routine clinical practice. 

Diagnosis and Diagnostic Criteria 

The Rosenberg-Patterson criteria6,9 are most often 

used for the diagnosis (Table 5). There are also a set 



Figure 3. Chest radiograph showing transient pulmonary opacities in the right lower lobe (left) ina 

patient with allergic bronchopulmonary aspergillosis that have spontaneously disappeared (right). 

of minimal diagnostic criteria for ABPA (Table 

5). 32,33 These criteria continue to be challenged and 

modified because there is lack of evidence on the 

number of criteria that should be present to make 

the diagnosis. The differentiation of patients with 

ABPA from patients with AH can also be problematic. 

Serum precipitins to A fumigatus is present in 

69 to 90% of patients with ABPA 23,112,116,126,127 but 

also in 9% of asthmatics. 112 Central bronchiectasis 

can be seen in patients with asthma without 

ABPA. 97–99 There are no cutoffs for total IgE levels 

with many using 1,000 IU/mL, 8,9,22,23,82,128–130 and 

others using 1,000 ng/mL (equivalent to 417 IU/ 

mL). 5,27,33,34 The total IgE levels may also be elevated 

in patients with AH without ABPA. As the 

understanding of ABPA has evolved, it is clear that 

patients with AH may present with less than the full 

complement of diagnostic criteria. 131 Thus, a cutoff 

value of 1,000 ng/mL IgE will probably lead to an 

overdiagnosis of ABPA. 131 The use of A fumigatus- 

Figure 4. HRCT images of different patients with allergic bronchopulmonary aspergillosis. Top right: 

bilateral central bronchiectasis with centrilobular nodules and tree-in-bud opacities in the left lung. Top 

left: bilateral central bronchiectasis with many mucus-filled bronchi. Bottom, left and right: images from 

the same patient show high-attenuation mucoid impaction. Bottom right: the mucoid impaction in the 

right lung is visually denser than the paraspinal skeletal muscle. 



Table 5—Criteria Used for the Diagnosis of ABPA 

Rosenberg-Patterson criteria 6,9 

Major criteria (mnemonic ARTEPICS) 

A Asthma 

R Roentgenographic fleeting pulmonary opacities 

T Skin test positive for Aspergillus (type I reaction, 

immediate cutaneous hyperreactivity) 

E Eosinophilia 

P Precipitating antibodies (IgG) in serum 

I IgE in serum elevated ( 1,000 IU/mL) 

C Central bronchiectasis 

S Serums A fumigatus-specific IgG and IgE (more than 

twice the value of pooled serum samples from patients with 

asthma who have Aspergillus hypersensitivity) 

Minor criteria 

Presence of Aspergillus in sputum 

Expectoration of brownish black mucus plugs 

Delayed skin reaction to Aspergillus antigen (type III 

reaction) 

The presence of six of eight major criteria makes the diagnosis 

almost certain; the disease is further classified as ABPA-S or 

ABPA-CB on the absence or presence of central 

bronchiectasis, respectively 

Minimal diagnostic criteria for ABPA 32 

Minimal ABPA-CB 

Asthma 

Immediate cutaneous hyperreactivity to Aspergillus antigens 


Elevated IgE 

Raised A fumigatus-specific IgG and IgE 

Minimal ABPA-S 

Asthma 

Immediate cutaneous hyperreactivity to Aspergillus antigens 

Transient pulmonary infiltrates on chest radiograph 

Elevated IgE 

Raised A fumigatus-specific IgG and IgE 

specific IgE and IgG levels can help in confirming 

the diagnosis of ABPA because values of IgG/IgE 

more than twice the pooled serum samples from 

patients with asthma are raised only in ABPA. 113,132 

We currently use a cutoff value of 1,000 IU/mL for 

the diagnosis of ABPA. 22,23 While investigating a 

patient with asthma, we first perform an Aspergillus 

skin test. Once it is positive, the total serum IgE 

levels are done. 131 If the value is 1,000 IU/mL, we 

perform the other tests (Fig 5). If the value is 

between 500 and 1,000 IU/mL, the next step is analysis 

of A fumigatus-specific IgE and IgG antibodies. If the 

levels are raised, the patient is followed up every 6 weeks 

with total IgE levels. If the absolute value rises 1,000 

IU/mL or there is a rising trend with clinical deterioration, 

the treatment is started. If the value is between 500 and 

1,000 IU/mL and IgE and IgG specific to A fumigatus are 

not raised, the patient is followed up with a yearly total 

IgE levels (Fig 5). 

Natural History 

The natural history of ABPA is not well characterized. 

9,128,133–136 An early diagnosis and initiation of 

systemic corticosteroids are essential to prevent irreversible 

damage. 137 The natural course of ABPA can 

be best understood if we recognize the two important 

classification schemes (Tables 6 and 7) of ABPA: 

(1) classification of ABPA into five stages as described 

by Patterson et al 8 , and (2) classification of 

ABPA into ABPA-S (seropositive ABPA) and ABPA-CB 

(ABPA with central bronchiectasis) described by 

Greenberger et al. 12 

Staging of ABPA: ABPA has been classified into 

five stages, but a patient does not necessarily 

progress from one stage to the other sequentially 

(Table 6). Patients in stage I or III (depending on 

whether or not the disorder has been previously 

diagnosed) are generally symptomatic with radiographic 

infiltrates, raised IgE levels, and elevated A 

fumigatus-specific IgG/IgE. 23 With glucocorticoid 

therapy, there is clearing of radiographic opacities 

with a 35 to 50% decline in IgE levels by 6 weeks 

that defines remission or stage II. The aim of 

glucocorticoid therapy is not normalization of total 

IgE levels because the immunologic process goes in 

remission with just 35 to 50% decline in IgE levels, 

and in many patients the IgE levels do not come to 

down to normal values. The test needs to be often 

repeated during therapy to determine the lowest 

level for an individual patient that serves as the 

baseline for that particular patient. Treatment is 

continued for 6 to 9 months, and if there are no 

exacerbations over the next 3 months after stopping 

therapy, we label it as “complete remission.” Patients 

in complete remission are followed up by serial IgE 

levels every 6 months for the first year and then 

annually. Even in patients with complete remission, 

the IgE levels decline to normal in only a minority of 

patients, 128,133 and the aim of glucocorticoid therapy 

is not achievement of normal IgE levels. 79 A complete 

remission does not imply a permanent remission 

because exacerbations can occur several years 

after remission. 135 Almost 25 to 50% of the patients 

have relapse/exacerbation of the disease, defined by 

doubling of the baseline IgE levels (stage III). 8,9,22 

Patients in stage IV require oral glucocorticoids for 

control of asthma (glucocorticoid-dependent asthma) 

or ABPA (glucocorticoid-dependent ABPA). 10,22 Patients 

in stage V are those with widespread bronchiectasis 

and varying degrees of pulmonary dysfunction. 

We define patients in stage V if they have 

hypercapnic respiratory failure (Pao 2 60 mm Hg 

and Paco 2 45 mm Hg) and/or cor pulmonale. 

Even in stage V ABPA, the disease can be clinically 

as well as immunologically active requiring longterm 

glucocorticoid therapy. 136,138 



Figure 5. Algorithm followed in the diagnostic workup for allergic bronchopulmonary aspergillosis in the author’s chest clinic. 

Radiologic Classification of ABPA: ABPA is classified 

as ABPA-S or ABPA-CB, respectively, depending 

on the absence or presence of bronchiectasis 

or as ABPA-S (mild), ABPA-CB (moderate), 

and ABPA-CB-ORF (other radiologic findings) 

(Table 7). Patients with ABPA-S probably represent 

the earliest stage of the disorder. It is believed 

that patients with ABPA-S have a milder 



clinical course and less severe immunologic findings 

when compared to ABPA-CB based on the 

inference of three studies (total of 124 patients). 

12,139,140 In the largest of these three studies 

(76 patients), only the A fumigatus-specific IgG 

levels were higher in patients with ABPA-CB 

compared to ABPA-S. Other immunologic parameters 

were not significantly different between the 

two groups. 12 In our study of 126 patients, the 

clinical, spirometric, and immunologic findings 

were not significantly different when classifying 

ABPA into ABPA-S and ABPA-CB or as ABPA-S, 

ABPA-CB, and ABPA-CB-ORF. 22 

However, the course of patients with ABPA-S is 

likely to be less severe when compared to those with 

ABPA-CB. In a multivariate analysis of 155 patients 

with ABPA, we demonstrated that the severity of 

bronchiectasis and presence of hyperattenuating 

mucoid impaction on HRCT-predicted relapses of 

ABPA and the severity of bronchiectasis was an 

independent predictor of failure to achieve longterm 

remission. 23 Thus it may not be important to 

stage the severity of ABPA based on the presence 

or absence of CB, but it remains prudent to 

diagnose and treat ABPA early to prevent the 

development of bronchiectasis because it in- 

Table 6—Stages of ABPA 8,22 

Stage Description Clinical Picture Radiologic Findings Immunologic Features 

I Acute phase Usually symptomatic, 

fever, weight loss, 

wheeze 

Normal or presence of 

radiologic opacities 

II Remission Asymptomatic Generally normal or significant 

resolution of radiologic 

opacities from the acute 

phase 

III Exacerbation Symptomatic as in acute Transient or fixed pulmonary 

phase 

opacities 

IV Glucocorticoid-dependent Symptomatic Transient or fixed pulmonary 

ABPA 

opacities 

V End-stage (fibrotic) 

ABPA 

Symptomatic, findings of 

fixed airway 

obstruction, severe 

pulmonary 

dysfunction, type II 

respiratory failure, cor 

pulmonale 

Evidence of bronchiectasis, 

pulmonary fibrosis, 

pulmonary hypertension 

IgE 1,000 IU/mL, raised 

specific IgG/IgE and 

precipitins to A fumigatus 

Usually 35–50% decline in IgE 

levels by 6 wk to 3 mo; we 

give additional label of 

“complete remission” if the 

patient did not have any 

additional ABPA exacerbations 

over the next 3 mo after 

stopping steroid therapy 

Doubling of IgE levels from 

baseline 

Two groups can be identified: 

one in whom IgE levels do not 

rise but require steroids for 

asthma control (glucocorticoiddependent 

asthma); the other 

in whom steroids are required 

to continually suppress the 

disease activity (glucocorticoiddependent 

ABPA) 

Serum IgE levels and specific 

immunoglobulins do not 

become normal in most 

patients, and even these 

patients can have frequent 

exacerbations 

creases the probability of a smoother course of this 

relapsing-remitting disorder. 

Management 

The management of ABPA includes two important 

aspects: institution of glucocorticoids to control the 

immunologic activity and close monitoring for detection 

of relapses. Another possible target is the use of 

antifungal agents to attenuate the fungal burden 

secondary to the fungal colonization in the airways. 

Systemic Glucocorticoid Therapy: Oral corticosteroids 

are the treatment of choice for ABPA. They not 

only suppress the immune hyperfunction but are also 

antiinflammatory. There are no data to guide the 

dose and duration of glucocorticoids, and different 

regimens of glucocorticoids have been used (Table 

8). The use of lower doses of glucocorticoids was 

associated with frequent relapses or corticosteroid 

dependence (45%). 9 We use a higher dosage of 

glucocorticoids for a longer duration and observed 

higher remission rates and a lower prevalence of 

glucocorticoid-dependent ABPA (13.5%). 22 This 

raises the possibility of a higher dose and prolonged 

duration of corticosteroid therapy being associated 



Table 7—Radiologic Classification of ABPA* 

Classification Features 

Greenberger et al12 classification 

ABPA-S All the diagnostic features of ABPA 

but no evidence of central 

bronchiectasis on HRCT. 

Patients with ABPA-S may be 

classified as Patterson stages I to 

IV. These patients may have 

recurrent exacerbations and may 

also be classified as stage III 

(ABPA-CB) All findings of ABPA including CB 

on HRCT. Patients with ABPA- 

CB may belong to any of the 

Patterson stages 

Kumar140 classification 

ABPA-S ABPA without CB 

ABPA-CB ABPA with CB 

ABPA-CB-ORF ABPA with CB other radiologic 

features such as pulmonary 

fibrosis, bleb, bullae, 

pneumothorax, parenchymal 

scarring, emphysematous change, 

multiple cyst, fibrocavitary 

lesions, aspergilloma, groundglass 

appearance, collapse, 

mediastinal lymph node, pleural 

effusion, and pleural thickening 

*Both the classification schemes believe that patients without CB and 

ORF have serologically milder disease, but it has been shown that 

there is no difference in clinical, spirometric, and serological 

severity between patients with and without bronchiectasis (see text 

for details). 

with better outcomes. However, there are no direct 

comparisons between the two regimens, and the 

selection is a matter of personal preference. The 

clinical effectiveness of steroid therapy is reflected 

by marked decreases in the patient’s total serum IgE 

levels (there seems to be no correlation between 

serum levels of A fumigatus-specific IgE levels and 

disease activity 141 ) along with symptom and radiographic 

improvements. The goal of therapy is not to 

attempt normalization of IgE levels but to decrease 

the IgE levels by 35 to 50%, which leads to clinical 

and radiographic improvement. One should also 

establish a stable serum level of total IgE to serve as 

a guide to future detection of relapse. 

Inhaled Corticosteroids: Although small case studies 

suggest some benefit of inhaled corticosteroids in 

the management of ABPA, 142–145 a double-blind multicenter 

placebo-controlled trial in 32 patients suggested 

no superiority over placebo. 146 We use inhaled 

corticosteroids only for the control of asthma once the 

oral prednisolone dose is reduced to 10 mg/day. 

Oral Itraconazole: Ketoconazole has been tried in 

the past 147 and has been replaced by the less toxic 

Table 8—Treatment Protocols for the Management of 

ABPA 

Oral glucocorticoids 

Regime 1 5 

Prednisolone, 0.5 mg/kg/d, for 1–2 wk, then on alternate days 

for 6–8 wk. Then taper by 5–10 mg every 2 wk and 

discontinue 

Repeat the total serum IgE concentration and chest 

radiograph in 6 to 8 wk 

Regime 2 22,113 

Prednisolone, 0.75 mg/kg, for 6 wk, 0.5 mg/kg for 6 wk, then 

tapered by 5 mg every 6 wk to continue for a total duration 

of at least 6 to 12 mo. The total IgE levels are repeated 

every 6 to 8 wk for 1 yr to determine the baseline IgE 

concentrations 

Follow-up and monitoring 

The patients are followed up with a medical history and 

physical examination, chest radiograph, and measurement of 

total IgE levels every 6 wk to demonstrate decline in IgE 

levels and clearing of the chest radiograph 

A 35% decline in IgE level signifies satisfactory response to 

therapy. Doubling of the baseline IgE value can signify a 

silent ABPA exacerbation 

If the patient cannot be tapered off prednisolone, the disease 

has evolved into stage IV. Management should be 

attempted with alternate-day prednisone with the least 

possible dose 

Monitor for adverse effects (eg, hypertension, secondary 

diabetes) 

Prophylaxis for osteoporosis: oral calcium and bisphosphonates 

Oral itraconazole 

Dose: 200 mg bid for 16 wk then once a day for 16 wk 

Indication: First relapse of ABPA or glucocorticoid-dependent 

ABPA 

Follow-up and monitoring 

Monitor for adverse effects (eg, nausea, vomiting, diarrhea, 

and elevated liver enzymes) 

Monitor for drug–drug interactions 

Monitor clinical response based on clinical course, 

radiography, and total IgE levels 

agent, itraconazole. 130,141,148–160 Only two randomized 

controlled studies (84 patients) have evaluated 

the role of itraconazole in ABPA. 130,156 Pooled analysis 

showed that itraconazole could significantly decrease 

the IgE levels by 25% when compared to 

placebo but did not cause significant improvement in 

lung function. 161 A major limitation was that neither 

of the studies reported long-term outcomes in 

ABPA. Thus longer term trials are required before a 

firm recommendation can be made for the use of 

itraconazole in ABPA. We currently use itraconazole 

only after the first relapse of ABPA despite glucocorticoid 

therapy or in patients with glucocorticoiddependent 

ABPA (Table 8). In the limited numbers 

of patients in whom we have used the drug, there 

was no observable advantage. 22 Itraconazole not only 

has numerous adverse effects, 162 but it also inhibits 

the metabolism of methylprednisolone (but not 

prednisolone) with resultant increased frequency of 



Table 9—Studies Describing Prevalence of AH and/or ABPA in Patients With CF 

Study Year Nature of Study Patients, No. AH in CF ABPA* in CF Diagnosis of AH† 

Mearns et al 184 

1967 Prospective 86 28/86 Skin test 

Allan et al 185 


Silverman et al 186 

1978 Prospective 48 17 Skin test 

Nelson et al 187 

1979 Prospective 46 18/46 5/46 Skin test 

Laufer et al 177 


Feanny et al 188 


Schonheyder et al 189 

1988 Prospective 200 10/200 

Zeaske et al 190 


Knutsen et al 176 


Nicolai et al 179 

1990 Prospective 148 58/148 Serology 

Simmonds et al 191 

1990 Prospective 137 8/137 

Hutcheson et al 192 


el-Dahr et al 193 

1994 Prospective 147 30/147 22/147 Serology 

Marchant et al 194 

1994 Retrospective 160 16/160 Skin test 

Mroueh and Spock 178 

1994 Retrospective 236 38/87 15/236 Skin test 

Becker et al 181 


Hutcheson et al 195 


Geller et al 182 

1999 Prospective 14,210 281/14,210 

Nepomuceno et al 153 

1999 Retrospective 172 16/172 

Cimon et al 196 


Mastella et al 174 

2000 Prospective 12,447 967/12,447 

Taccetti et al 197 

2000 Prospective 3,089 191/3,089 

Ritz et al 180 

2005 Prospective 160 20/160 11/160 Serology 

Skov et al 183 


Almeida et al 198 


Kraemer et al 173 

2006 Prospective 122 16/122 

Chotirmall et al 199 


Rapaka and Kolls 200 


* ABPA: Studies have used different inclusion criteria for diagnosing ABPA. See text for further details. 

† AH: Defined as immediate cutaneous hypersensitivity to Aspergillus antigen or a positive specific IgE in serum against A fumigatus 

(radioallergosorbent test class 2) and/or increased specific IgE in serum against rAsp f1 9.6 EU/mL, with normal values for rAsp f4 ( 8.4 

EU/mL) and rAsp f6 ( 7.2 EU/mL) 

steroid side effects including adrenal insufficiency. 163 

Adrenal suppression has also been reported with the 

concomitant use of itraconazole and inhaled budesonide. 

164,165 

Other Therapies: There is a single patient case 

report of ABPA treated with inhaled amphotericin 

and budesonide. 166 Similarly, there is another case 

record on the use of omalizumab for the management 

of ABPA. 167 One author has also used pulse 

doses of IV methylprednisolone for the treatment of 

severe ABPA. 168 Recently, voriconazole has also 

been tried in the treatment of ABPA. 169–171 

Differential Diagnosis and Complications 

The disorder needs to be differentiated from the 

following conditions: Aspergillus hypersensitive 

bronchial asthma, pulmonary tuberculosis in endemic 

areas, community-acquired pneumonia (especially 

acute presentations), and other inflammatory 

pulmonary disorders such as eosinophilic pneumonia, 

bronchocentric granulomatosis, and Churg- 

Strauss syndrome. The complications of ABPA in- 

clude recurrent asthma exacerbations and, if 

untreated, the development of bronchiectasis with 

subsequent pulmonary hypertension and respiratory 

failure. In fact, this is the reason why routine screening 

is recommended in bronchial asthma to prevent 

the complications just described. 

ABPA in Special Situations 

ABPA Complicating CF: The association of ABPA 

and CF was first reported in 1965. 172 The occurrence 

of ABPA in CF is associated with deterioration 

of lung function, higher rates of microbial colonization, 

pneumothorax, massive hemoptysis, and poorer 

nutritional status. 153,173,174 A key element in the 

immunopathogenesis may be exposure to high levels 

of Aspergillus allergens due to abnormal mucus 

properties. 175 The recognition of ABPA in CF can be 

difficult because ABPA shares many clinical characteristics 

with poorly controlled CF lung disease. 

Presence of wheezing, pulmonary infiltrates, bronchiectasis, 

and mucus plugging are common manifestations 

of CF-related pulmonary disease without 

ABPA. The prevalence of AH in patients with CF 



has been reported between 29% and 53%, 176–180 and 

the prevalence of ABPA as 1 to 15%. Atopy seems to 

be an important risk factor for ABPA in CF, with 

ABPA observed in 22% of atopic patients but only 

2% of nonatopic patients. 153,181–183 

To determine the prevalence of AH/ABPA in CF, 

a systematic search was performed. The search 

yielded 28 studies (16 studies [1,391 patients] describing 

the prevalence of AH in CF and 23 

studies [32,589 patients] describing the prevalence 

of ABPA in CF) that have described the prevalence 

of AH and/or ABPA in patients with CF 

(Table 9). 153,173,174,176–200 A proportion metaanalysis of 

these studies suggested the prevalence of AH in CF 

of 34% (95% confidence interval, 27 to 41) and the 

prevalence of ABPA of 7.8% (95% confidence interval, 

5.8 to 10) using a random effects model [Figs 6 

and 7]. There was no uniformity in the diagnostic 

criteria between different studies with varying criteria 

used for diagnosis of AH and ABPA. This fact has 

also been previously reported in a questionnairebased 

study, which revealed a considerable variability 

in the criteria used for the diagnosis of ABPA in 

CF. 201 Therefore, prospective reporting of cases with 

uniform criteria would be the only way to reliably 

identify the true prevalence of ABPA in CF. 

Although a high proportion of CF patients develop 

sensitization to A fumigatus, many demonstrate a 

spontaneous decline in many immunologic parameters, 

including IgE levels. 192 The diagnosis of ABPA 

Figure 6. Proportion metaanalysis showing the prevalence of Aspergillus hypersensitivity in patients with cystic fibrosis (random effects 

model). 



Figure 7. Proportion metaanalysis showing the prevalence of allergic bronchopulmonary aspergillosis in patients with CF (random 

effects model). 

in CF should not be based solely on serology and 

skin test results, and prolonged testing might be 

required to make a definite diagnosis (Table 10). The 

treatment of ABPA in CF is not very different from 

that of ABPA in bronchial asthma, except minimal 

data are available to formulate conclusive treatment 

recommendations for ABPA in CF. The treatment 

issues are further complicated because pulmonary 

exacerbations in a patient with ABPA and CF could 

be related to ABPA or pulmonary infection, and 



Table 10—Consensus Conference Proposed Diagnostic 

and Screening Criteria for ABPA in CF 202 

Classic diagnostic criteria 

1. Acute or subacute clinical deterioration (cough, wheeze, and 

other pulmonary symptoms) not explained by another etiology 

2. Serum total IgE levels 1,000 IU/mL 

3. Immediate cutaneous reactivity to Aspergillus or presence of 

serum IgE antibody to A fumigatus 

4. Precipitating antibodies to A fumigatus or serum IgG antibody 

to A fumigatus 

5. New or recent abnormalities on chest radiograph or chest CT 

scan that have not cleared with antibiotics and standard 

physiotherapy 

Minimal diagnostic criteria 

1. Acute or subacute clinical deterioration (cough, wheeze, and 

other pulmonary symptoms) not explained by another etiology 

2. Total serum IgE levels 500 IU/mL. If total IgE level is 200– 

500 IU/mL, repeat testing in 1–3 mo is recommended 

3. Immediate cutaneous reactivity to Aspergillus or presence of 

serum IgE antibody to A fumigatus 

4. One of the following: (1) precipitins to A fumigatus or 

demonstration of IgG antibody to A fumigatus; or (2) new or 

recent abnormalities on chest radiography (on chest radiography 

or chest CT scan that have not cleared with antibiotics and 

standard physiotherapy) 

Screening for ABPA in CF 

1. Maintain a high level of suspicion for ABPA in patients with CF 

2. Determine the total serum IgE levels annually. If the total 

serum IgE levels is 500 IU/mL, perform A fumigatus skin test 

or use an IgE antibody to A fumigatus. If results are positive, 

consider diagnosis on the basis of minimal criteria 

3. If the total serum IgE levels is 200–500 IU/mL, repeat the 

measurement if there is increased suspicion for ABPA and perform 

further diagnostic tests (immediate skin test reactivity to A 

fumigatus, IgE antibody to A fumigatus, A fumigatus precipitins, or 

serum IgG antibody to A fumigatus, and chest radiography) 

hence continuous assessment may be required over 

months with repeat performance of all the serologic 

investigations for ABPA before a decision to treat an 

individual case is made. 202 

ABPA Without Bronchial Asthma: ABPA may 

occasionally develop in an individual without preexisting 

asthma. We have performed a systematic 

MEDLINE search for the occurrence of ABPA 

without bronchial asthma. 100 In total they included 

36 cases reported across the globe; two cases demonstrated 

bronchodilator reversibility, 203 and one 

showed airway hyperresponsiveness to methacholine 

challenge. 204 Most of the cases demonstrated hypersensitivity 

to A fumigatus, but three cases 

showed hypersensitivity to Helminthosporium, 203 

and one case each to Aspergillus niger. 205,206 Because 

of the absence of bronchial asthma, these 

cases are often mistaken initially for other pulmonary 

disorders like bronchogenic carcinoma 206–208 

or pulmonary tuberculosis. 100 

ABPA Complicating Other Conditions: Occasionally 

ABPA has been reported to complicate other 

lung diseases like idiopathic bronchiectasis, 209 

post-tubercular bronchiectasis, 210 bronchiectasis 

secondary to Kartagener syndrome, 211 COPD, 212 

and in patients with chronic granulomatous disease 

and hyper IgE syndrome. 213 However, these 

are case reports or small case studies, and larger 

observations are required to definitely establish an 

association. 

Coexistence of ABPA and Aspergilloma: The serologic 

findings of ABPA have also been reported in 

patients with aspergilloma 214–224 and chronic necrotizing 

pulmonary aspergillosis. 225 This ABPA-like 

syndrome probably represents a true hypersensitivity 

reaction consequent to the colonization of Aspergillus 

in long-standing pulmonary cavities and the 

continuous release of Aspergillus antigens that leads 

to immunologic activation. 214,215 Most patients show 

a brisk response to glucocorticoids. 214–217,224 

Allergic Bronchopulmonary Mycosis: Allergic 

bronchopulmonary mycosis is the occurrence of an 

ABPA-like syndrome due to non-A fumigatus fungal 

organisms. A variety of fungal agents (Table 11) have 

been reported to cause this syndrome, but the frequency 

is far less when compared to ABPA. 218,226–240 

ABPA and Allergic Aspergillus Sinusitis: Allergic 

Aspergillus sinusitis (AAS) is a clinical entity in which 

mucoid impaction akin to that of ABPA occurs in the 

paranasal sinuses. 241 The pathogenesis is also similar 

to ABPA and represents an allergic hypersensitivity 

response to the presence of fungi within the sinus 

cavity. 242 The patient is often asymptomatic or can 

manifest with symptoms of nasal obstruction, rhinor- 

Table 11—Fungi Implicated in the Causation of 

Allergic Bronchopulmonary Mycosis 

Fungi Study/Year 

A niger Sharma et al 218 /1985 

Helminthosporium spp Dolan et al 226 /1970 

Penicillium spp Sahn and Lakshminarayan 227 /1973 

Aspergillus ochraceus Novey and Wells 228 /1978 

Stemphylium spp Benatar et al 229 /1980 

Aspergillus terreus Laham et al 230 /1981 

Drechslera spp McAleer et al 231 /1981 

Torulopsis spp Patterson et al 232 /1982 

Mucor-like spp Patterson et al 232 /1982 

Candida spp Akiyama et al 234 /1984 

Pseudallescheria spp Lake et al 235 /1990 

Bipolaris spp Lake et al 236 /1991 

Curvularia spp Lake et al 236 /1991 

Schizophyllum spp Kamei et al 237 /1994 

Fusarium spp Backman et al 238 /1995 

Cladosporium spp Moreno-Ancillo et al 239 /1996 

Saccharomyces spp Ogawa et al 240 /2004 



hea, headache, and epistaxis. Occasionally, the 

allergic fungal sinusitis may extend into adjacent 

spaces such as the orbit and manifest as proptosis. 

243 Although in many patients with ABPA, 

sinusitis can often be radiologically demonstrated, 

it may not be possible to confirm the diagnosis of 

AAS because many patients decline to undergo the 

diagnostic procedures required to establish the 

diagnosis. We currently label the patients with 

ABPA as having concomitant AAS if there is 

combination of hyperattenuating mucus and/or 

bony erosion on a paranasal CT scan. Treatment is 

initiated for ABPA with patients receiving additional 

intranasal glucocorticoids. If the symptoms 

persist or are troublesome, surgical management 

may be required for the management of AAS. 

Conclusions 

A high index of suspicion for ABPA should be 

maintained while managing any patient with bronchial 

asthma whatever the severity or the level of 

control. Host immunologic responses are central to 

the pathogenesis, and they are the primary determinants 

of the clinical, biologic, pathologic, and radiologic 

features of this disorder. ABPA may precede 

the clinical recognition of the disorder for many 

years or even decades, and it is often misdiagnosed as 

a variety of pulmonary diseases. Because a patient 

with ABPA can be minimally symptomatic or asymptomatic, 

all patients with bronchial asthma should be 

routinely screened with an Aspergillus skin test. In 

patients with Aspergillus hypersensitivity, further 

immunologic studies are warranted to diagnose 

ABPA before the development of bronchiectasis 

because bronchiectasis is a poor prognostic marker 

in the natural history of this disease. 

ACKNOWLEDGMENT: The author wishes to thank Dr. Amanjit 

Bal, Assistant Professor, Department of Histopathology, 

PGIMER, Chandigarh for providing the histopathology photographs. 

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