Allergic bronchopulmonary aspergillosis (ABPA) occurs in patients with asthma or cystic fibrosis, and results in pulmonary infiltrates, tenacious mucus plugs that harbor hyphae of Aspergillus fumigatus, elevations of total serum immunoglobulin E concentration and peripheral blood and sputum eosinophilia. Bronchiectasis is an irreversible complication of ABPA. The key to early diagnosis is to consider ABPA in anyone with asthma or cystic fibrosis and with a positive skin test result for Aspergillus, and/or recurrent infiltrates on radiographs. The differential diagnosis for ABPA in patients with asthma includes diseases in which there is an overlap of asthma, peripheral blood eosinophilia, and radiographic infiltrates. Examples include chronic eosinophilic pneumonia, Churg-Strauss syndrome, drug-induced pulmonary infiltrates, infection with a parasite, asthma with atelectasis, and lymphoma. Mucus plugging that causes a “tree in bud” pattern on computerized tomography examination of the lungs may be from ABPA or other conditions, such as nontuberculous (atypical) mycobacteria (Mycobacteria avium‐Mycobacteria intracellulare complex). Prednisone is indicated to clear pulmonary infiltrates, and a usual course is for 3 months. Itraconazole and voriconazole are adjunctive, and drug-drug interactions must be considered because azoles decrease elimination of various medications. Although not familial in most patients, presentation of Aspergillus fumigatus f1 (Asp f1) antigen is restricted to specific major histocompatibility complex (MHC) class II molecules, Human Leukocyte Antigen-DR2 (HLA-DR2), and HLA-DR5. There is an increased number of CD4+ T-helper type 2 lymphocytes in bronchoalveolar lavage, and A. fumigatus can serve as a growth factor of eosinophils potentiating the effects of interleukin (IL) 3, IL-5, and Granulocyte-colony stimulating factor (G-CSF). Eosinophils interact directly with A. fumigatus spores and generate extracellular traps, which can injure the bronchial epithelium.