Pulmonary aspergillosis is mainly caused by Aspergillus fumigatus. The fungus is often parasitic in the upper respiratory tract, chronic disease patients with extremely low immunity to cause the disease. Aspergillus is widely present in nature, the air has its spores everywhere, in autumn and winter and rainy season, storage of grain and grass fever mold more. Aspergillus spores do not necessarily cause disease, such as a large number of inhaled may cause acute tracheobronchitis or pneumonia. Aspergillus endotoxin makes tissue necrosis, lesions can be infiltrative, solid, cavernous, peribronchiolitis or corn-like diffuse lesions. The diagnosis of pulmonary aspergillosis depends on tissue culture (biopsy specimens of diseased organs) and histopathological examination, which can be seen as sharp-angled branches separated by non-pigmented mycelium; tissue or body fluid culture with Aspergillus spp. growth. If the culture of respiratory specimens is positive, smears see mycelium for at least 2 consecutive times; or there are characteristic changes in lung, brain, sinus CT or X-ray; patients who are severely immunocompromised should be suspected of Aspergillosis. Immunosuppressed host invasive Aspergillosis its bronchoalveolar lavage fluid smear, culture and/or antigen assay has good specificity and positive predictive value. Antigen skin test with Aspergillus leachate, allergic patients have tachyphylaxis, indicating the presence of IgE antibodies. Serum Aspergillus antibody determination and blood, urine, cerebrospinal fluid and alveolar lavage fluid Aspergillus galactomannan determination and PCR determination of blood Aspergillus DNA is also helpful in the diagnosis of the disease. There are three main clinical types of pulmonary aspergillosis: I. Invasive pulmonary aspergillosis is the most common type, severe lung tissue destruction, difficult to treat. Pulmonary aspergillosis is mostly confined granulomatous or extensive purulent pneumonia with abscess formation. The lesions show acute coagulative necrosis with necrotizing vasculitis, thrombosis and bacterial emboli, and even involvement of the pleura. Symptoms include dry cough, chest pain, hemoptysis in some patients, shortness of breath and dyspnea, and even respiratory failure when the lesion is extensive. The characteristic imaging manifestations are wedge-shaped shadow or cavity with pleural base on X-ray chest radiograph; halo sign on chest CT in early stage, i.e. pulmonary nodular shadow (edema or hemorrhage) surrounded by hypointense shadow (ischemia), and crescentic sign in later stage. Some patients may have central nervous system infection and show signs and symptoms of the central nervous system. Amphotericin B is the treatment of choice, especially for severe life-threatening infections at the highest tolerated dose possible [1-1.5 mg/(kg/d)]. If the patient cannot tolerate it, it is advisable to start with a small dose for the first time, 0.lmg/kg per day dissolved in 5% glucose solution in a slow, light-protected sedative drip, increasing by 5-l0mg day by day to the maximum tolerated dose and then maintain treatment. There is no uniform opinion on the course of treatment and total dose, which can be given individually according to the extent of the patient’s disease, response to treatment, underlying disease or immune status. The addition of appropriate amounts of heparin to the drops helps prevent thrombophlebitis. The main adverse reactions are chills, fever, panic, back pain and impairment of liver and kidney function. However, moderate renal impairment during administration is not an indication for discontinuation of the drug. Amphotericin B lipid complex, which is less nephrotoxic, is mainly suitable for patients with existing renal impairment or nephrotoxicity after using amphotericin B at a dose of 5mg/(kg/d). Voriconazole, caspofungin and micafungin can also be used. Second, Aspergilloma, also known as varicella, the disease is often secondary to bronchial cysts, bronchiectasis, lung abscesses and tuberculosis cavities. It is Aspergillus multiplying and accumulating in the original cavity of chronic lung disease, and coalescing with fibrin, mucus and cellular debris into Aspergilloma. Aspergilloma does not invade the tissue, but can develop into invasive pulmonary aspergillosis. There can be irritating cough, often repeated hemoptysis, and even life-threatening hemoptysis. X-rays of the chest show a ball of shadow in the original chronic cavity, which moves within the cavity with changes in body position. Aspergilloma treatment is mainly to prevent life-threatening hemoptysis, if conditions permit, surgery should be performed. Bronchial artery embolization can be used for the treatment of hemoptysis. Endobronchial and pus cavity injection of antifungal drugs or oral itraconazole may be effective. Allergic bronchopulmonary aspergillosis (ABPA) is an airway hyperreactive disease caused by Aspergillus fumigatus. Aspergillus allergic to a large number of spores after inhalation, blocking the small bronchi, causing transient episodes of pulmonary atelectasis and wheezing, but also cause repeated wandering infiltration of the lungs. Patients wheezing, chills, fever, fatigue, irritating cough, coughing brownish yellow pus sputum, occasionally with blood. The sputum is full of eosinophils and Aspergillus filaments and is positive for Aspergillus fumigatus culture. Asthma-like episodes are the prominent clinical manifestation of the disease, and the usual antispasmodic and antiasthmatic drugs are ineffective, with an increase in peripheral blood eosinophils. A typical chest X-ray shows transient solid or non-dilated upper lobes, which may occur bilaterally. Central bronchodilator signs such as the “ring sign” and “orbital sign” are present. Acute ABPA requires glucocorticoids, starting with prednisone 0.5 mg/(kg/d) and changing to every other day after 1 week. Anti-trypanosomal therapy may be effective in patients with severe disease. Chronic ABPA glucocorticosteroid dose 7.5-10mg/d. The dose and duration of treatment are determined on a case-by-case basis. Beta2-agonists or inhaled glucocorticoids may be used as appropriate.