Allergic
Bronchopulmonary Aspergillosis
Erin Walker MacKintosh, MD, FAAP, and Margaret Rosenfeld, MD, MPH
Introduction/Etiology/Epidemiology
•Allergic bronchopulmonary aspergillosis (ABPA) is an immunologic pulmonary disorder caused by immunoglobulin E (IgE)–mediated hypersensitivity to the fungus Aspergillus fumigatus, primarily in patients with asthma or cystic fibrosis.
•A fumigatus is a ubiquitous environmental fungus; it cannot be transmitted person to person.
—It is typically found in dust, soil, or decaying organic matter, such as compost.
•Risk for ABPA is multifactorial and includes genetic predisposition and environmental exposures.
•ABPA typically manifests as poorly controlled asthma with productive cough and recurrent pulmonary infiltrates; it can progress to bronchiectasis and pulmonary fibrosis.
•More than 4 million patients are affected worldwide; the disorder is widely underdiagnosed.
—Prevalence of ABPA ranges from 1% to 3.5% in people with asthma.
—Regional differences exist in the United States, due in part to different diagnostic criteria and frequency of screening of asymptomatic patients.
Pathophysiology
•A fumigatus, a common environmental fungus, is inhaled into the lung.
•In healthy, normal lungs, inhaled spores are cleared from the airway. The spores are immunologically inert and do not lead to sensitization.
•Defective clearance (seen in asthma and cystic fibrosis) of inhaled spores allows A fumigatus to germinate into hyphae.
•The hyphal form is proinflammatory, activating innate and adaptive type 2 T helper (Th2) cell immune response.
—Type 1 T helper (Th1) cells primarily promote cell-mediated immunity, and Th2 cells more typically promote allergic responses.
—Macrophages recognize surface antigens on the hyphal forms and secrete proinflammatory cytokines.
—While a normal lung would elicit a Th1 response, leading to Aspergillus-specific T cells, a lung susceptible to ABPA (due to genetic risk factors) is more likely to respond with Th2 response. This creates inflammation and leads to IgE synthesis and influx of eosinophils and other inflammatory cells.
•Typically, hyphal forms would be cleared by neutrophils, but defects in innate and adaptive immunity (genetic risk factors, poor mucociliary clearance) can lead to persistence of hyphal forms in the airway.
—Genetic mutations and polymorphisms associated with ABPA have been identified in multiple genes (including HLA, surfactant protein A2, TLR9, mannose-binding lectin, IL4Rα, IL10, TGBβ, CFTR, and CHIT1); the clinical significance of these findings is not yet clear.
•Patients develop Aspergillus sensitization, identified by either positive skin test results or increased Aspergillus-specific IgE.
•Prolonged positive reinforcement of antigen-mediated inflammatory cascade via persistent exposure to Aspergillus antigen leads to progressive parenchymal and airway damage.
Clinical Features
•Poorly controlled asthma
•Airflow obstruction, wheezing
•Recurrent pulmonary infiltrates
•Bronchiectasis
•Hemoptysis
•Productive cough, sometimes producing brown or black mucus plugs
•Can include low-grade fevers, weight loss, malaise, and fatigue with acute exacerbations
•Can be asymptomatic except for declining forced expiratory volume in 1 second values
•With prolonged and poorly managed disease, can develop clubbing, pulmonary hypertension, and cor pulmonale
Differential Diagnosis
•Poorly controlled asthma
•Pneumonia: viral, bacterial, eosinophilic
•Hypersensitivity pneumonitis
•Retained foreign body
•Pulmonary tuberculosis
•Chronic pulmonary aspergillosis
—Pulmonary aspergilloma
—Chronic cavitary pulmonary aspergillosis
—Chronic fibrosing pulmonary aspergillosis
•Severe asthma with fungal sensitization is similar to ABPA, but without bronchiectasis and mucus plugging, with an IgE level <1,000 IU/mL (<2.4 mg/L).
•Allergic Aspergillus sinusitis is mucoid impaction of the sinuses with a mechanism similar to ABPA.
•Allergic bronchopulmonary mycosis is an ABPA-like syndrome caused by fungi other than Aspergillus, with <150 cases reported.
Diagnostic Considerations
•ABPA is typically diagnosed and managed by a pediatric pulmonologist or allergist. Thus, when a patient is not responding adequately to the usual treatment of asthma, or if there is suspected or confirmed ABPA, the child should be referred.
•There are varying diagnostic criteria in use. The International Society for Human and Animal Mycology working group is trying to create a unified diagnostic paradigm (see Box 44-1).
•Additional studies frequently used, but not required for diagnosis, are as follows.
—Sputum cultures for A fumigatus are neither sensitive nor specific but can be useful in terms of susceptibilities if positive.
—Pulmonary function tests can be used to trend response to treatment, but in some cases can have normal findings in confirmed ABPA.
—Chest computed tomographic findings may include
▪Bronchiectasis: a complication, not diagnostic criteria; usually central, can be peripheral
▪Mucus impaction, classically described as “finger in glove” owing to mucus filling the airways
▪Mosaic attenuation (air trapping)
▪Centrilobular nodules
▪Tree-in-bud opacities
▪Pleuropulmonary fibrosis
▪Rarely: effusions, pulmonary masses, miliary nodular opacities, perihilar opacities simulating hilar adenopathy
Treatment
•Goals of treatment include control of symptoms, prevention and/ or treatment of acute exacerbations, and arresting development of bronchiectasis and fibrosis.
—Consensus exists that patients with ABPA and mucoid impaction or changes to lung function or symptomatic patients should be treated.
—There is not consensus on treating asymptomatic patients.
•The target of treatment is Th2 cell–mediated immune response.
Box 44-1. Diagnostic Criteria Proposed by the International Society for Human and Animal Mycology Working Group
Obligatory Criteria
•Underlying diagnosis of asthma
•Positive A fumigatus–specific IgE or Aspergillus-specific skin test result
—Skin test is 90% sensitive, but ≤40% of asthmatics without ABPA may also have a positive result .
•Total IgE level >1,000 IU/mL (>2 .4 mg/L) or >2,400 ng/mL
—Consensus has not been achieved on this cutoff, and ABPA may be diagnosed with a lower IgE level if other diagnostic criteria are fulfilled .
—Levels may decrease spontaneously or with treatment, so the first or highest level available should be used .
—Increasing levels may be seen in exacerbations .
Other Criteria (must have 2 out of 3)
•Positive precipitating or IgG antibodies against A fumigatus
•Radiographic pulmonary opacities consistent with ABPA
•Total eosinophil count >500 cells/µL (0 .5 x 109/L) in patients who have not yet received steroids (may be historical)
ABPA, allergic bronchopulmonary aspergillosis; IgE, immunoglobulin E; IgG, immunoglobulin G .
From Agarwal R, Chakrabarti A, Shah A, et al . Allergic bronchopulmonary aspergillosis: review of literature and proposal of new diagnostic and classification criteria . Clin Exp Allergy. 2013;43(8):850–873 . © 2013 John Wiley & Sons Ltd .
•Standard treatments
—The mainstay of treatment is systemic corticosteroids to suppress immune activity.
▪There are inadequate studies to guide dose or duration; many different protocols are in use.
▪A typical initial treatment regimen is prednisone 0.5 mg/kg/d for 1–2 weeks, then tapering over 8–10 weeks.
▪Half of patients relapse when steroids are tapered.
▪Ten percent to 45% of patients become steroid dependent.
—If the patient relapses or if the response to steroids is inadequate, antifungal medication is used to decrease fungal load as a steroid-sparing therapy.
▪Therapy is generally continued for minimum of 3–6 months.
▪Evidence supports the use of antifungals in chronic ABPA but not for treatment of acute exacerbations.
▪No evidence exists for antifungals as monotherapy (ie, without systemic corticosteroids), although clinical trials are underway.
▪Drug level monitoring is required to reduce the risk of toxicity and assess the risk of azole resistance and reduced effectiveness if levels are too low.
•Monitoring response to treatment includes total IgE level (unlikely to normalize but should decrease), symptom assessment, and pulmonary function tests.
•Other treatments have insufficient evidence but may be considered in refractory cases or those with absolute contraindications to systemic corticosteroids and/or itraconazole.
—Omalizumab is a monoclonal antibody to IgE. There is mounting but still insufficient evidence for use as mainstay therapy, and it may be cost prohibitive.
—Inhaled corticosteroids do not appear sufficient for treatment of ABPA. If used for control of underlying asthma, consider that effects increase when used concurrently with itraconazole (there is a risk for cushingoid effects and adrenal insufficiency).
—Inhaled amphotericin: There are case reports of use in cystic fibrosis– associated ABPA, but there is not strong evidence.
—Pulse doses of intravenous methylprednisolone: There is insufficient evidence to recommend it.
—Avoidance of activities that provide a high burden of spore inhalation (farming, gardening, composting, building renovations, cleaning dusty environments) may reduce risk, but the evidence is insufficient.
Prognosis
•Minimal data are available for the prognostication of treated ABPA.
—Patients can have prolonged remissions, but this does not imply cure.
—ABPA requires lifelong monitoring.
—If untreated, ABPA can progress to severe bronchiectasis, respiratory failure, and cor pulmonale.
•Complications
—Recurrent exacerbations may be caused by airway inflammation or mucus plugging.
▪Prevent exacerbations with judicious use of steroids and azoles; treat acutely with steroid bursts.
—Large airway collapse due to mucus plugging can occur in acute hypoxemic respiratory failure, necessitating therapeutic bronchoscopy.
—Bronchiectasis can eventually develop. It is irreversible and a prognostic indicator for recurrence of exacerbations.
•What Is Allergic Bronchopulmonary Aspergillosis? (American Thoracic Society). www.thoracic.org/patients/patient-resources/resources/ allergic-bronchopulm-aspergillosis.pdf
Clinical Pearl
•When a patient is not responding adequately to the usual treatment of asthma, or if there is suspected or confirmed ABPA, the child should be referred to a pediatric pulmonologist or allergist.
CHAPTER 25: DIAGNOSIS OF ASTHMA
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CHAPTER 26: TOBACCO SMOKE EXPOSURE AND CHILDREN;
CHAPTER 27: PREVENTING AND TREATING TOBACCO DEPENDENCE
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•U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General. 2012
CHAPTER 28: NONPHARMACOLOGICAL MANAGEMENT AND USE OF COMPLEMENTARY AND ALTERNATIVE MEDICINE THERAPIES FOR ASTHMA
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CHAPTER 29: ALLERGIC RHINITIS
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CHAPTER 30: ASTHMA GUIDELINES: OVERVIEW;
CHAPTER 31: ASTHMA GUIDELINES: MANAGEMENT OF ACUTE ASTHMA;
CHAPTER 32: ASTHMA GUIDELINES: MANAGEMENT OF CHRONIC ASTHMA
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CHAPTER 33: PHARMACOLOGICAL MANAGEMENT: SHORT-ACTING ꞵ2-ADRENERGIC AGONISTS
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CHAPTER 34: PHARMACOLOGICAL MANAGEMENT: LONG-ACTING ꞵ2-ADRENERGIC AGONISTS
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CHAPTER 35: PHARMACOLOGICAL MANAGEMENT: INHALED CORTICOSTEROIDS
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•Adams N, Bestall J, Jones PW. Budesonide for chronic asthma in children and adults. Cochrane Database Syst Rev. 2001;(4)
•Derendorf H, Nave R, Drollmann A, Cerasoli F, Wurst W. Relevance of pharmaco-kinetics and pharmacodynamics of inhaled corticosteroids to asthma. Eur Respir J. 2006;28(5):1042–1050
•Kapadia CR, Nebesio TD, Myers SE, et al; Drugs and Therapeutics Committee of the Pediatric Endocrine Society. Endocrine effects of inhaled corticosteroids in children. JAMA Pediatr. 2016;170(2):163–170
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•Lemanske RF Jr, Mauger DT, Sorkness CA, et al; Childhood Asthma Research and Education (CARE) Network of the National Heart, Lung, and Blood Institute. Step-up therapy for children with uncontrolled asthma receiving inhaled corticosteroids. N Engl J Med. 2010;362(11):975–985
CHAPTER 36: PHARMACOLOGICAL MANAGEMENT: LEUKOTRIENE RECEPTOR AGONISTS
•Kelly H, Sorkness CA. Asthma. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L, eds. Pharmacotherapy: A Pathophysiologic Approach. 9th ed. New York, NY: McGraw-Hill; 2014
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•Chauhan BF, Ducharme FM. Anti-leukotriene agents compared to inhaled corticosteroids in the management of recurrent and/or chronic asthma in adults and children. Cochrane Database Syst Rev. 2012;(5)
CHAPTER 37: PHARMACOLOGICAL MANAGEMENT: ANTICHOLINERGIC AGENTS
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•Tin W, Wiswell TE. Adjunctive therapies in chronic lung disease: examining the evidence. Semin Fetal Neonatal Med. 2008;13(1):44–52
CHAPTER 38: PHARMACOLOGICAL MANAGEMENT: SYSTEMIC CORTICOSTEROIDS
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•Campbell RM Jr. VEPTR: past experience and the future of VEPTR principles. Eur Spine J. 2013;22(Suppl 2):S106–S117
•Mayer OH. Management of thoracic insufficiency syndrome. Curr Opin Pediatr. 2009;21(3):333–343
•Mayer OH. Chest wall hypoplasia—principles and treatment. Paediatr Respir Rev. 2015;16(1):30–34
•Redding GJ. Primary thoraco-spinal disorders of childhood. Paediatr Respir Rev. 2015;16(1):25–29
CHAPTER 39: PHARMACOLOGICAL MANAGEMENT: ANTI-IMMUNOGLOBULIN E THERAPY
•Chipps BE, Lanier B, Milgrom H, et al. Omalizumab in children with uncontrolled allergic asthma: review of clinical trial and real-world experience. J Allergy Clin Immunol. 2017;139(5):1431–1444
•Wright LS, Phipatanakul W. Treatment of moderate to severe pediatric asthma: Omalizumab and potential future use of monoclonal antibodies. Ann Allergy Asthma Immunol. 2016;117(1):17–20
•Humbert M, Busse W, Hanania NA, et al. Omalizumab in asthma: an update on recent developments. J Allergy Clin Immunol Pract. 2014;2(5):525–536
CHAPTER 40: IMMUNOTHERAPY
•Cox L, Nelson H, Lockey R, et al. Allergen immunotherapy: a practice parameter third update. J Allergy Clin Immunol. 2011;127(1 Suppl):S1–S55
•Burks AW, Calderon MA, Casale T, et al. Update on allergy immunotherapy: American Academy of Allergy, Asthma & Immunology/European Academy of Allergy and Clinical Immunology/PRACTALL consensus report. J Allergy Clin Immunol. 2013;131(5):1288–1296 y Calderon MA, Alves B, Jacobson M, Hurwitz B, Sheikh A, Durham S. Allergen injection immunotherapy for seasonal allergic rhinitis. Cochrane Database Syst Rev. 2007;(1):CD001936
•Nelson HS. Subcutaneous immunotherapy versus sublingual immunotherapy: which is more effective? J Allergy Clin Immunol Pract. 2014;2(2):144–149, quiz 150–151
•Akdis M, Akdis CA. Mechanisms of allergen-specific immunotherapy: multiple suppressor factors at work in immune tolerance to allergens. J Allergy Clin Immunol. 2014;133(3):621–631
CHAPTER 41: EXERCISE-INDUCED BRONCHOCONSTRICTION
•Krafczyk MA, Asplund CA. Exercise-induced bronchoconstriction: diagnosis and management. Am Fam Physician. 2011;84(4):427–434
•Koh MS, Tee A, Lasserton TJ, Irving LB. Inhaled corticosteroids compared to placebo for prevention of exercise induced bronchoconstriction. Cochrane Databse Syst Rev. 2007;(3):CD002739
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•Parsons JP, Hallstrand TS. An Official American Thoracic Society clinical practice guideline: exercise-induced bronchoconstriction. Am J Respir Crit Care Med. 2013;87:1016–1027
•Parsons JP, Mastronarde JG. Exercise-induced bronchoconstriction in athletes. Chest. 2005;128(6):3966–3974
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•Rundell KW, Slee JB. Exercise and other indirect challenges to demonstrate asthma or exercise-induced bronchoconstriction in athletes. J Allergy Clin Immunol. 2008; 122(2):238–246, quiz 247–248
CHAPTER 42: RECURRENT CROUP AND BRONCHITIS
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•Joshi V, Malik V, Mirza O, Kumar BN. Fifteen-minute consultation: structured approach to management of a child with recurrent croup. Arch Dis Child Educ Pract Ed. 2014;99(3):90–93
•Rankin I, Wang SM, Waters A, Clement WA, Kubba H. The management of recurrent croup in children. J Laryngol Otol. 2013;127(5):494–500
•Atmaca S, Unal R, Seşen T, Kiliçarslan H, Unal A. Laryngeal foreign body mistreated as recurrent laryngitis and croup for one year. Turk J Pediatr. 2009;51(1):65–66
•Karkos PD, Leong SC, Apostolidou MT, Apostolidis T. Laryngeal manifestations and pediatric laryngopharyngeal reflux. Am J Otolaryngol. 2006;27(3):200–203
•Foskey G Jr, Singer J. Artificial nail aspiration masquerading as refractory croup. Pediatr Emerg Care. 2005;21(8):523–526 y Perkins JA, Duke W, Chen E, Manning S. Emerging concepts in airway infantile hemangioma assessment and management. Otolaryngol Head Neck Surg. 2009; 141(2):207–212
•Zgherea D, Pagala S, Mendiratta M, Marcus MG, Shelov SP, Kazachkov M. Bronchoscopic findings in children with chronic wet cough. Pediatrics. 2012; 129(2):e364–e369
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CHAPTER 43: RECURRENT WHEEZING IN INFANTS, TODDLERS, AND PRESCHOOLERS
•Maclennan C, Hutchinson P, Holdsworth S, Bardin PG, Freezer NJ. Airway inflammation in asymptomatic children with episodic wheeze. Pediatr Pulmonol. 2006;41(6):577–583
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CHAPTER 44: ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS IN ASTHMA
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•Agarwal R, Aggarwal AN, Dhooria S, et al. A randomised trial of glucocorticoids in acute-stage allergic bronchopulmonary aspergillosis complicating asthma. Eur Respir J. 2016;47(2):490–498
•Moss RB. Treating allergic bronchopulmonary aspergillosis: the way forward. Eur Respir J. 2016;47(2):385–387
•Knutsen AP. Allergic bronchopulmonary aspergillosis in asthma. Expert Rev Clin Immunol. 2017;13(1):11–14
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