Pulmonary candidiasis (PCD) is an infectious disease of the lungs caused by Candida spp. It mainly includes lesions associated with Candida infection of the lungs and bronchi, such as bronchitis, bronchopneumonia, pneumonia, lung abscess, and allergic pulmonary lesions, but not fungal parasites. Pulmonary Candida infection can be either a primary infection of the lung caused by direct invasion of the pathogenic organism or a secondary infection of the lung caused by hematogenous dissemination of Candidaemia to the lung, the latter being the manifestation of invasive candidiasis (IC) in the lung. The natural defense mechanisms of the lungs are somewhat resistant to invasion of lung tissue by Candida spp. Even in critically ill patients treated with mechanical ventilation, positive cultures of Candida from airway secretions may simply be Candida colonization rather than infection. Therefore, the current definition of Candida pneumonia is the presence of histopathological changes of Candida invasion of the lung in addition to the corresponding clinical manifestations, as well as a positive culture of Candida in the lung tissue, so the true diagnosis of Candida pneumonia and lung abscess is very rare, and the exact incidence data is lacking, which is yet to be confirmed by further studies. Recently, the results of a multicenter retrospective study led by Prof. Liu Yuning in China suggest that pulmonary candidiasis is not rare, and its incidence is second only to that of pulmonary aspergillosis, among the seven common pulmonary fungal diseases. Intra-airway colonization by Candida spp. and/or contamination of respiratory secretions with oropharyngeal Candida is extremely common, and a positive culture of Candida from respiratory secretions alone without other evidence of invasive candidiasis cannot be used as an indication for starting antifungal therapy in patients with fever of unknown origin. Several prospective and retrospective studies (including autopsies) have consistently shown that a positive culture of Candida from respiratory secretions (including bronchoalveolar lavage fluid) has no definite clinical significance. I. Risk factors for pulmonary candidiasis Patients with pulmonary candidiasis usually have risk factors that are extensive, and the most common high-risk factors can be divided into two main categories, host factors and factors of medical origin. Host factors include advanced age, previous Candida colonization (>1 site), burns or severe trauma, combination of underlying diseases such as malignancy, diabetes mellitus, severe pancreatitis, severe disease such as APACHE II score >10, malnutrition, gastric acid suppression, neutrophil deficiency, previous invasive candidiasis, etc.; medical factors include admission to ICU, long-term heavy use of broad-spectrum antibiotics, and use of various indwelling catheters such as central venous catheters, parenteral nutrition therapy, mechanical ventilation (>48 hours), abdominal surgery or cardiac surgery, prosthetic implants, and treatment with immunosuppressive agents (including adrenal glucocorticoids, chemotherapeutic agents, and immunomodulators). It is now recognized that most of the above risk factors are common confounding factors in the hospital setting or ICU setting and individually are not very helpful in determining IC risk, whereas it is important to look at them as a continuous whole, with the likelihood of infection increasing exponentially when 2 or more risk factors are present simultaneously. Categorization of the above risk factors reveals that they are mainly due to disruption of the human mucosal barrier for various reasons (especially disruption of the skin, the GI barrier and barrier disruption due to indwelling catheters); dysbiosis due to broad-spectrum antibiotic use (killing Candida-inhibiting bacteria); previous invasive candidiasis or/and presence of Candida colonization; various treatments such as underlying diseases or medications resulting in immunosuppression. Some authors have also proposed a clinical score to help the physician determine whether a patient has Candida infection or colonization to facilitate early empirical treatment. For example, Leon et al. proposed the Candida score to identify the most likely invasive Candidiasis and to facilitate early antifungal treatment of ICU patients. The strategy is based on a large, prospective, multicenter study that analyzes Candida colonization and potential risk factors on a weekly basis. The study included 1669 non-neutropenic patients, 97 of whom had confirmed invasive candidiasis. logistic regression analysis identified four independent risk factors: multifocal Candida colonization, surgery, parenteral intravenous nutrition, and severe sepsis. Candidiasis was scored as follows: severe sepsis 2, surgery 1, parenteral intravenous nutrition 1, and multilocus Candida colonization 1. The score is defined as 2.5, and the likelihood of confirming a Candida infection when the individual patient score is >2.5 is 7.75 times greater than when the score is ≤2.5. The method has a sensitivity and specificity of 81% and 74%. Risk factor stratification helps to more precisely select patients who would truly benefit from preventive or empirical (preemptive) treatment. There are two routes of infection for pulmonary candidiasis: the inhalation route, in which Candida colonizing the oral and upper airways is inhaled into the lower airways and alveoli when the body’s defense mechanisms are weakened, resulting in primary bronchopulmonary candidiasis; and the blood route, which causes invasive infection of deep tissues and organs and infects lung tissue as secondary pulmonary candidiasis. The defense function of human body against Candida requires a complete immune system, especially neutrophils (PMNs). Neutrophils first respond to Candida invasion, followed by macrophage infiltration and granuloma formation. When the immune function of the body is low, Candida can grow and multiply in large numbers locally, and change from yeast phase to mycelial phase with increased virulence, leading to infection and even to disseminated candidiasis. Second, clinical manifestations (a) clinical types 1. according to the lesion site is divided into: (1) bronchitis type: lesions involving bronchi and surrounding tissues, but did not invade the lung parenchyma, imaging examination shows increased lung texture, thickening, blurring; (2) pneumonia type: Candida invades the alveoli, causing acute, subacute or chronic inflammatory changes in the lung parenchyma, imaging shows signs of bronchopneumonia or lobar pneumonia. 2. According to the route of infection is divided into: (1) primary (inhalation) Candida pneumonia: refers to the invasive Candida infection that occurs and is confined to the lungs; some patients may also have hematogenous dissemination. (2) Secondary Candida pneumonia: refers to pulmonary lesions caused by hematogenous dissemination of Candida bloodstream infection. (3) Other types: special types such as allergic, pulmonary Candida globules and Candida pulmonary cavity. (2) Clinical symptoms: The clinical manifestations of pulmonary candidiasis are non-specific. 1. Systemic manifestations: The main manifestations are fever of unknown cause, ineffective antibacterial treatment or reappearance of fever after symptoms have improved. There may be thrush, rash, muscle aches, and in the presence of Candidaemia, multiple small abscesses of liver and spleen, chorioretinitis, abnormal liver function, unexplained mental disorder, and hypotension and shock. 2. Pulmonary symptoms: bronchitis type has mild symptoms, may have cough, cough a small amount of white mucous sputum; pneumonia type clinical symptoms depend on the pathogenesis (primary or secondary), host state and the scope of pneumonia, etc., mostly acute pneumonia or with sepsis performance, cough, sputum is little and sticky or mucus colloid-like or sputum with blood, not easy to cough up, may be accompanied by dyspnea, chest pain, etc. Allergic pulmonary candidiasis resembles the manifestations of allergic rhinitis or asthma, with frequent runny nose, sneezing, chest tightness, shortness of breath, etc. (C) Signs: Signs are often less frequent. In some patients, thrush or scattered white membranes can be seen in the oropharynx, dry moist rales can be heard in the lungs, and severe patients can have cyanosis of the lips and mouth. Signs of allergic pulmonary candidiasis are similar to allergic rhinitis or asthma, with pale nasal mucosa and audible croup in the lungs.