Allergic bronchopulmonary aspergillosis

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Allergic bronchopulmonary aspergillosis
Chest Xray of allergic bronchopulmonary aspergillosis showing left-sided perihilar opacity (blue arrow) along with non-homogeneous infiltrates (transient pulmonary infiltrates indicated by red arrows) in all zones of both lung fields
SpecialtyInfectious disease
SymptomsWheezing, cough including coughing up blood, fever, tiredness, weight loss[1]
CausesAspergillus exposure[1]
Diagnostic methodBased on symptoms, medical imaging, and blood tests[2][3]
Differential diagnosisPneumonia, Churg-Strauss syndrome[2]
TreatmentAntifungal medication, corticosteroids[1]
Frequency2% of people with asthma[2]

Allergic bronchopulmonary aspergillosis (ABPA) is an allergic reaction to the fungus Aspergillus, after it has been inhaled.[1][4] Symptoms may include wheezing, cough including coughing up blood, fever, tiredness, and weight loss.[1] Complications may include bronchiectasis—a condition marked by abnormally dilated airways.[2]

Most people breathe in Aspergillus spores without getting sick.[5] Risk factors include asthma, cystic fibrosis, and being immunocompromised.[3] The underlying mechanism involves inflammation due to an abnormal immune response which results in increased mucus production.[2] The diagnosis may be supported by chest X-ray, CT scan, increased eosinophils, IgE levels of greater than 1,000 IU/mL, or a positive skin allergy test to A. fumigatus.[2] It is a type of aspergillosis.[5]

Treatment is generally with the antifungal medication itraconazole and corticosteroids such as prednisone.[1] Other agents used may include amphotericin B and omalizumab.[2] In about half of people the disease recurs and repeated treatment is requires.[1] ABPA affects about 1 to 4 million people.[4] It occurs in about 2% of people with asthma and up to 15% of people with cystic fibrosis.[2]

Signs and symptoms

Almost all people have asthma,[6] and present with wheezing (usually episodic in nature), coughing, shortness of breath and exercise intolerance (especially in those with cystic fibrosis).[7][8] Moderate and severe cases have symptoms suggestive of bronchiectasis, in particular thick sputum production (often containing brown mucus plugs), as well as symptoms mirroring recurrent infection such as pleuritic chest pain and fever. Patients with asthma and symptoms of ongoing infection, who do not respond to antibiotic treatment, should be suspected of ABPA.[7]


The conidiophore of the fungal organism Aspergillus fumigatus

Aspergillus spores are small (2–3 μm in diameter) and can penetrate deep into the respiratory system to the alveolar level.[9][10] In healthy people, innate and adaptive immune responses are triggered by various immune cells (notably neutrophils, resident alveolar macrophages and dendritic cells) drawn to the site of infection by numerous inflammatory cytokines and neutrophilic attractants (such as CXCR2 receptor ligands).[11] In this situation, mucociliary clearance is initiated and spores are successfully phagocytosed, clearing the infection from the host.[9][12]

In people with predisposing lung diseases—such as persistent asthma or cystic fibrosis (or rarer diseases such as chronic granulomatous disease or Hyper-IgE syndrome)—several factors lead to an increased risk of ABPA.[13] These include immune factors (such as atopy or immunogenic HLA-restricted phenotypes),[14][15] as well as genetic factors (such as CFTR gene mutations in both asthmatics and cystic fibrosis patients and a ZNF77 mutation resulting in a premature stop codon in asthmatics and ABPA patients).[16][12][17] By allowing Aspergillus spores to persist in pulmonary tissues, it permits successful germination which leads to hyphae growing in mucus plugs.

There are hypersensitivity responses, both a type I response (atopic, with formation of immunoglobulin E, or IgE) and a type III hypersensitivity response (with formation of immunoglobulin G, or IgG).[12][18] The reaction of IgE with Aspergillus antigens results in mast cell degranulation with bronchoconstriction and increased capillary permeability.[19] Immune complexes (a type III reaction) and inflammatory cells are deposited within the mucous membranes of the airways, leading to necrosis (tissue death) and eosinophilic infiltration.[12] Type 2 T helper cells appear to play an important role in ABPA due to an increased sensitivity to interleukin (IL) 4 and IL-5. These cytokines up-regulate mast cell degranulation, exacerbating respiratory decline.[20][21][22]

Aspergillus also utilises a number of factors to continue evading host responses, notably the use of proteolytic enzymes that interrupt IgG antibodies aimed towards it. Another important feature is its ability to interact and integrate with epithelial surfaces, which results in massive pro-inflammatory counter-response by the immune system involving IL-6, IL-8 and MCP-1 (a CCL2 receptor ligand). Proteases released by both the fungus and neutrophils induce further injury to the respiratory epithelium, leading to initiation of repair mechanisms (such as an influx of serum and extracellular matrix (ECM) proteins) at the site of infection. Aspergillus spores and hyphae can interact with ECM proteins, and it is hypothesised that this process facilitates the binding of spores to damaged respiratory sites.[12][23]

As concentrations of Aspergillus proteases increase, the immunological effect switches from pro-inflammatory to inhibitory, and further reduces phagocytic ability to clear Aspergillus. Ultimately, repeated acute episodes lead to wider scale damage of pulmonary structures (parenchyma) and function via irreversible lung remodelling. Left untreated, this manifests as progressive bronchiectasis and pulmonary fibrosis that is often seen in the upper lobes, and can give rise to a similar radiological appearance to that produced by tuberculosis.[23][24]


a) Bronchoscopy showed mucus plug (black arrow) b) infiltration of eosinophils in mucus plug

The exact criteria for the diagnosis of ABPA are not yet universally agreed upon, though working groups have proposed specific guidelines.[13][25] Minimal criteria include five factors: the presence of asthma and/or cystic fibrosis, a positive skin test to Aspergillus sp., total serum IgE > 416 IU/mL (or kU/L), an increased Aspergillus species–specific IgE and IgG antibodies, and the presence of infiltrates on a chest X-ray.[26][27]

ABPA should be suspected in patients with a predisposing lung disease—most commonly asthma or cystic fibrosis— and is often associated with chronic airway limitation (CAL). Patients generally present with symptoms of recurrent infection such as fever, but do not respond to conventional antibiotic therapy. Poorly-controlled asthma is a common finding, with a case series only finding 19% of ABPA patients with well-controlled asthma. Wheezing and hemoptysis (coughing up blood) are common features, and mucus plugging is seen in 31–69% of patients.[13]

Blood tests

The first stage involves exposing the skin to Aspergillus fumigatus antigens; an immediate reaction is hallmark of ABPA.[28] The test should be performed first by skin prick testing, and if negative followed with an intradermal injection. The overall sensitivity of the procedure is around 90%, though up to 40% of asthmatic patients without ABPA can still show some sensitivity to Aspergillus antigens (a phenomenon likely linked to a less severe form of ABPA termed severe asthma with fungal sensitization (SAFS)).[13]

Serum blood tests are an important marker of disease severity and are also useful for the primary diagnosis of ABPA. When serum IgE is normal (and patients are not being treated by glucocorticoid medications), ABPA is excluded as the cause of symptoms. A raised IgE increases suspicion, though there is no universally accepted cut-off value. Values can be stated in international units (IU/mL) or ng/mL, where 1 IU is equal to 2.4 ng/mL. Since studies began documenting IgE levels in ABPA during the 1970s, various cut-offs between 833 and 1000 IU/mL have been employed to both exclude ABPA and to warrant further serological testing. The current consensus is that a cut-off of 1000 IU/mL should be employed, as lower values are encountered in SAFS and asthmatic sensitization.[13]

IgG antibody precipitin testing from serum is useful, as positive results are found in between 69 and 90% of patients, though also in 10% of asthmatics with and without SAFS. Therefore, it must be used in conjunction with other tests. Various forms exist, including enzyme-linked immunosorbent assay (ELISA) and fluorescent enzyme immunoassay (FEIA). Both are more sensitive than conventional counterimmunoelectrophoresis. IgG may not be entirely specific for ABPA, as high levels are also found in chronic pulmonary aspergillosis (CPA) alongside more severe radiological findings.[13][29]

Until recently, peripheral eosinophilia (high eosinophil counts) was considered partly indicative of ABPA. More recent studies show that only 40% of ABPA sufferers present with eosinophilia, and hence a low eosinophil count does not necessarily exclude ABPA; for example patients undergoing steroid therapy have lower eosinophil counts.[13]

Medical imaging

Consolidation and mucoid impaction are the most commonly described radiological features described in ABPA literature, though much of the evidence for consolidation comes from before the development of computed tomography (CT) scans. Tramline shadowing, finger-in-glove opacities and ‘toothpaste shadows’ are also prevalent findings.[30]

When utilising high-resolution CT scans, there can be a better assessment of the distribution and pattern of bronchiectasis within the lungs, and hence this is the tool of choice in the radiological diagnosis of ABPA. Central (confined to medial two-thirds of the medial half of the lung) bronchiectasis that peripherally tapers bronchi is considered a requirement for ABPA pathophysiology, though in up to 43% of cases there is a considerable extension to the periphery of the lung.[7]

Mucoid impaction of the upper and lower airways is a common finding.[7] Plugs are hypodense but appear on CT with high attenuation (over 70 Hounsfield units[31]) in up to 20% of patients. Where present it is a strong diagnostic factor of ABPA and distinguishes symptoms from other causes of bronchiectasis.[13]

CT scans may more rarely reveal mosaic-appearance attenuation, centrilobular lung nodules, tree-in-bud opacities and pleuropulmonary fibrosis (a finding consistent with CPA, a disease with ABPA as a known precursor).[7] Rarely other manifestations can be seen on CT scans, including military nodular opacities, perihilar opacities (that mimic hilar lymphadenopathy), pleural effusions and pulmonary masses. Cavitation and aspergilloma are rarer findings, not exceeding 20% of patients, and likely represent a shift from ABPA to CPA if accompanied by pleural thickening or fibrocavitary disease.[13]


Culturing fungi from sputum is a supportive test in the diagnosis of ABPA, but is not 100% specific for ABPA as A. fumigatus is ubiquitous and commonly isolated from lung expectorant in other diseases. Nevertheless, between 40 and 60% of patients do have positive cultures depending on the number of samples taken.[13]


New criteria by the ABPA Complicated Asthma ISHAM Working Group suggests a 6-stage criteria for the diagnosis of ABPA, though this is yet to be formalised into official guidelines.[13] This would replace the current gold standard staging protocol devised by Patterson and colleagues.[25] Stage 0 would represent an asymptomatic form of ABPA, with controlled asthma but still fulfilling the fundamental diagnostic requirements of a positive skin test with elevated total IgE (>1000 IU/mL). Stage 6 is an advanced ABPA, with the presence of type II respiratory failure or pulmonary heart disease, with radiological evidence of severe fibrosis consistent with ABPA on a high-resolution CT scan. It must be diagnosed after excluding the other, reversible causes of acute respiratory failure.[13]


Underlying disease must be controlled to prevent exacerbation and worsening of ABPA, and in most this consists of managing their asthma or CF. Any other co-morbidities, such as sinusitis or rhinitis, should also be addressed.[32]


Corticosteroids such as prednisone are often used; however, evidence is limited. There is some evidence that acute-onset ABPA is improved by corticosteroid. Concerns with long term corticosteroids include immune dysfunction and metabolic disorders.[32][33]

While the benefits of corticosteroids in the short term are notable, and improve quality of life scores, there are cases of ABPA converting to invasive aspergillosis with this treatment. Furthermore, in concurrent use with itraconazole, there is potential for drug interaction and the induction of Cushing syndrome. Metabolic disorders, such as diabetes mellitus and osteoporosis, can also be induced.[32][33]

In order to mitigate these risks, corticosteroid doses are decreased biweekly assuming no further progression of disease after each reduction. When no exacerbations from the disease are seen within three months after discontinuing corticosteroids, the person is considered to be in complete remission. The exception to this rule is people who are diagnosed with advanced ABPA; in this case, removing corticosteroids almost always results in exacerbation and these patients are continued on low-dose corticosteroids (preferably on an alternate-day schedule).[32][33]

Serum IgE can be used to guide treatment, and levels are checked every 6–8 weeks after steroid treatment commences, followed by every 8 weeks for one year. This allows for a determination of baseline IgE levels, though it's important to note that most patients do not entirely reduce IgE levels to baseline. Chest X-ray or CT scans are performed after 1–2 months of treatment to ensure infiltrates are resolving.[32][33]


Efforts to decrease the use of steroids include using antifungals. The strongest evidence is for itraconazole 200 mg twice daily for four months.[3] Using itraconazole appears to outweigh the risk from long-term and high-dose prednisone. Newer triazole drugs—such as posaconazole or voriconazole—have not yet been studied in-depth.[32][33]


There are limited national and international studies into the burden of ABPA, made more difficult by a non-standardized diagnostic criteria. Estimates of between 0.5 and 3.5% have been made for ABPA burden in asthma,[34][35] and 1–17.7% in CF.[34][36] Five national cohorts, detecting ABPA prevalence in asthma (based on GINA estimates),[37] were used in a recent meta-analysis to produce an estimate of the global burden of ABPA complicating asthma. From 193 million asthma sufferers worldwide, ABPA prevalence in asthma is estimated between the extremes of 1.35–6.77 million sufferers, using 0.7–3.5% attrition rates. A compromise at 2.5% attrition has also been proposed, placing global burden at around 4.8 million people affected. The Eastern Mediterranean region had the lowest estimated prevalence, with a predicted case burden of 351,000; collectively, the Americas had the highest predicted burden at 1,461,000 cases. These are likely underestimates of total prevalence, given the exclusion of CF patients and children from the study, as well as diagnostic testing being limited in less developed regions.[35]


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