| disease | Pulmonary Aspergillosis |
| alias | Pulmonary Aspergillosis |
The causative agent of pulmonary aspergillosis is primarily Aspergillus fumigatus, with a minority being Aspergillus flavus, Aspergillus terreus, Aspergillus niger, Aspergillus clavatus, Aspergillus nidulans, and Aspergillus versicolor. From 1949 to the end of 1988, over 300 cases of respiratory aspergillosis were reported in China, yet the total number before 1972 was only 47 cases. The vast majority of pulmonary aspergillosis cases are secondary infections, with primary cases being extremely rare. Clinically, the disease is generally classified into three types: aspergilloma, allergic bronchopulmonary aspergillosis (ABPA), and invasive pulmonary aspergillosis (IPA).
bubble_chart Pathogenesis
Aspergilloma is the most common type. Aspergillus often colonizes cavities formed by chronic lung diseases such as pulmonary tuberculosis, bronchial cysts, lung cancer, and sarcoidosis. The cavity walls and surrounding lung tissue are partially destroyed, with intra-alveolar hemorrhage, infiltration of numerous chronic inflammatory cells, and many proliferating small arteries and veins showing tumor-like dilation, generally without hyphal invasion. The cavity contains a yellowish-brown, friable spherical mass with pigmented deposits on the cut surface, consisting of clusters of septate branching hyphae mixed with abundant eosinophilic amorphous material and red blood cells. ABPA results from a combined effect of type I and type III hypersensitivity reactions. Inhaled short-chain Aspergillus spores become trapped in the mucus of larger segmental bronchi, forming hyphae. Their antigens bind specifically to IgE-sensitized mast cells, releasing mediators that cause bronchospasm, increased bronchial mucosal permeability, and antigen entry into tissues, leading to pulmonary and blood eosinophilia. Additionally, Aspergillus antigens combine with IgG antibodies to form immune complexes, which, with complement involvement, trigger chronic inflammation in the bronchi and surrounding lung tissue, resulting in bronchial destruction, dilation, and pulmonary fibrosis. The bronchial walls and lung parenchyma show eosinophil and monocyte infiltration with granuloma formation, and the lumen contains Aspergillus hyphae without tissue invasion. IPA occurs in patients with chronic debilitating diseases, dysbiosis, or impaired immune function. Aspergillus in the upper respiratory tract invades lung tissue, progressing to necrotizing hemorrhagic pneumonia, which may lead to suppuration, forming multiple abscesses or granulomas. The lesion margins may exhibit small septic emboli. Aspergillus invasion of pulmonary vessels causes hematogenous dissemination, affecting other organs throughout the body.
bubble_chart Clinical ManifestationsPatients with aspergilloma have no obvious systemic symptoms but may experience hemoptysis and cough. A solitary crescent-shaped lucent area with a spherical lesion in the lung is its typical X-ray manifestation.
ABPA generally occurs in individuals with an atopic constitution, presenting as recurrent episodes of wheezing, fever, cough, expectoration of brown mucus plugs, and hemoptysis. Physical examination reveals widespread wheezing in both lungs, with fine moist rales in areas of pulmonary infiltration. Chest X-rays show infiltrative lesions distributed in lobes or segments, often migratory; lung hyperinflation or atelectasis of segments or lobes due to bronchial mucus plugs without interlobar fissure displacement. Long-term recurrent episodes can lead to central bronchiectasis, with affected segmental or subsegmental bronchi showing cystic dilation while the distal portions remain normal. Shadows resembling tramlines, parallel lines, rings, bands, toothpaste, or finger cots are also commonly observed. Blood eosinophilia is present, and serum IgE levels are elevated. Intradermal testing with Aspergillus extract may yield a dual antagonistic response: within 15–20 minutes, a wheal and flare reaction appears, subsiding in about 0.5–2 hours (Type I reaction); upon re-examination at 4–10 hours, an Arthus reaction appears at the test site, subsiding in about 24–36 hours (Type III reaction). Patients have Aspergillus-specific precipitins, with a positive rate of 92% when tested using concentrated serum samples.
IPA patients exhibit severe illness, with fever, cough, purulent sputum, chest pain, hemoptysis, dyspnea, and symptoms and signs corresponding to dissemination to other organs. Physical examination reveals dry and moist rales in the lungs. Early X-rays may show localized or bilateral multifocal infiltrates or nodular shadows, which often rapidly expand and coalesce into consolidation or necrosis, forming cavities; or sudden large, wedge-shaped shadows with the base facing the pleura, resembling "mild" pulmonary infarction. A few cases may present with pleural effusion.
Aspirating secretions from the deep bronchi, finding hyphae on smears, and obtaining multiple positive cultures aid in diagnosis. The typical X-ray features of aspergilloma have diagnostic significance. Positive aspergillus antigen intradermal tests and serum precipitation tests are of diagnostic value. The diagnosis of allergic bronchopulmonary aspergillosis can be made when there is episodic bronchial asthma, peripheral blood eosinophilia, elevated serum IgE, pulmonary infiltrates on X-ray, and the presence of aspergillus hyphae on smears or positive aspergillus cultures from secretions aspirated via fiberoptic bronchoscopy. Fluoroscopy-guided transbronchial lung biopsy via fiberoptic bronchoscopy has definitive diagnostic value for aspergilloma and invasive pulmonary aspergillosis.
bubble_chart Treatment Measures
Aspergilloma is generally ineffective against antifungal drug therapy, and surgical treatment should be pursued.
For patients with allergic bronchopulmonary aspergillosis, although antifungal drugs such as amphotericin B administered via tracheal instillation or aerosol inhalation have certain efficacy in eliminating bronchial aspergillus, recurrence is common. Currently, corticosteroids are considered the most effective treatment for this condition, as they can suppress allergic reactions, reduce sputum production, and create an unfavorable environment for aspergillus colonization in the bronchial lumen. Generally, oral prednisone at 0.5 mg/kg/day helps with the absorption of pulmonary infiltrates. After two weeks, the dosage can be adjusted to every other day, maintained for at least three months. Amphotericin B can also be combined, with aerosol inhalation yielding satisfactory results. Typically, dexamethasone 2.5 mg and amphotericin B 5 mg are added to 10 ml of saline for aerosol inhalation twice daily for one month. For refractory cases, bronchoscopic lavage should be performed to aspirate viscous secretions and maintain airway patency, thereby enhancing drug efficacy.
