Pulmonary aspergillosis is a group of acute and chronic pulmonary diseases caused by Aspergillus infection or inhalation of Aspergillus antigens, including allergic, parasitic and invasive pulmonary aspergillosis (IPA), reflecting different host immune states. IPA is the most serious type of the disease and is extremely difficult to diagnose and treat. 1, pathogenesis Aspergillus belongs to the fungal world of the subphylum Hemiptera, with 18 groups of 132 species, at least 20 species can cause human infection, such as Aspergillus fumigatus, Aspergillus flavus, Aspergillus niger and Aspergillus terreus. Among them, Aspergillus fumigatus is the most common and can cause 90% of infections. The lung is the most common primary focus of infection, followed by the central nervous system, other sites of infection are: skin, sinuses, pharynx, digestive tract, liver and spleen. Aspergillus grows only in the form of mycelium, which is separated, 2-5μm in diameter, 45° bifurcation, and has the ability of tissue invasion. 2 , epidemiology and risk factors Aspergillus is widely distributed in nature in organic matter necrosis, moldy grain, feed, water, soil and air. Its infection lacks regional, but is a certain seasonality. Generally autumn and winter rainy season is more frequent, but bone marrow transplant patients in the summer is common. Aspergillus pulmonarius is mainly an exogenous infection, the vast majority is caused by the inhalation of a large number of Aspergillus spores through the respiratory tract, and very few are caused by traumatic inoculation. Hospital infection is an important factor, especially hospitals adjacent to construction sites or the use of Aspergillus contaminated air conditioning systems, can cause small outbreaks of epidemics within the hospital. Aspergillus is a conditionally pathogenic bacteria, when the immune function is suppressed or impaired susceptible to infection. 1996 a large sample of European autopsies showed that the incidence of IPA has increased nearly 14 times in the last 12 years. Common predisposing factors include: bone marrow transplantation, malignant hematological diseases, solid organ transplantation, and AIDS [3]. Neutropenia is the most important risk factor, and COPD is receiving increasing attention as a predisposing factor for IPA, mainly in patients treated with large amounts of hormones and multiple broad-spectrum antibiotics. 3 , typing and clinical manifestations Pulmonary aspergillosis can be clinically classified into [4]: (i) non-pathogenic saprophytic colonisation; (ii) pulmonary aspergilloma; (iii) allergic-mediated pulmonary aspergillosis, including aspergillus asthma, allergic bronchopulmonary aspergillosis (allergic bronchopulmonary aspergillosis) bronchopulmonary aspergillosis (ABPA), exogenous allergic alveolitis; ④ invasive pulmonary aspergillosis (IPA). ABPA manifests as wheezing, elevated blood eosinophils and Aspergillus-specific IgE, and is a hypersensitivity reaction of the body to Aspergillus antigens; Aspergillus globulus is a typical manifestation of parasitic aspergillosis, usually seen in immunocompetent individuals; clinical symptoms of IPA are mainly persistent fever, cough, chest pain, and in severe cases, respiratory distress. Fever is common and often occurs in conjunction with broad-spectrum antibiotic therapy; in addition, fever is often masked by the application of hormones. Mycelia of Aspergillus tend to invade blood vessels, forming local emboli and bleeding, causing hemoptysis. IPA is a common cause of hemoptysis in neutrophil deficient individuals. Pleural effusion is uncommon. 4, imaging features of IPA include: single or multiple nodules, segmental or subsegmental solid lesions, diffuse hairy glass shadow (often progressing to solid lesions), and cavities. HRCT can be more helpful in the diagnosis of IPA. Nodules are the most common CT manifestation of IPA. Infiltration of blood vessels by mycelia may form emboli and hemorrhagic bands, which appear as a halo sign around the nodule and are a specific early manifestation of IPA. Necrosis and shrinkage of lung tissue may form a half-moon shaped air shadow around a lung nodule, called the “crescent air sign”, which appears later than the “halo sign”. The halo sign combined with the air meniscus has a sensitivity of >80% for the diagnosis of IPA [6]. However, these signs are not specific to IPA and can also be seen in Trichophyton rubrum, Pseudomallei infection and BOOP, Kaposi’s sarcoma, etc. HRCT should be routinely performed in patients suspected of IPA. 5 .Diagnosis IPA is diagnosed in 3 levels: 1）Confirmed diagnosis (proven): histopathological finding of characteristic mycelium with/without positive tissue culture from the same site; 2）Clinical diagnosis (probable): the clinical manifestations are consistent, and there are 2 sputum cultures or 1 BAL culture or 1 brush culture positive, or 1 BAL in which characteristic mycelium is found, or The international consensus on the diagnosis of invasive fungal infections in 2002 re-emphasized that the sensitivity of Aspergillus culture is poor, so the “gold standard” for confirming the diagnosis is a positive histopathological finding, which does not necessarily require culture to confirm. Culture is not necessarily needed to confirm. The group recommends the use of Aspergillus antigen Galactomannan (GM) test as a clinical diagnostic basis, which requires >1 positive test result due to the presence of certain false positives. 6 , Treatment In patients with immunodeficiency, IPA is often fatal. Empirical antifungal therapy should be started promptly when IPA is clinically suspected, and the effectiveness of treatment depends on the ability to diagnose early, the degree of dissemination, the intensity of antifungal therapy, and the immune status of the host. Polyenes, triazoles, and echinocandins are the recognized antifungal agents [8]. Traditionally, amphotericin B (or liposomes) has been used for treatment, but itraconazole is now usually chosen, and voriconazole and caspofungin may also be used in critically ill patients, combined with 2 antifungal drugs if necessary. A temporary increase in intrapulmonary lesions while the patient is recovering neutrophils should not be mistaken for failure of antifungal therapy. The antifungal course should be followed until clinical and imaging changes disappear, cultures turn negative, and the underlying disease is controlled.