Pneumocystis carinii, previously known as Pneumocystis carinii (PC), is now classified as a fungus, and pulmonary infections caused by PC are called Pneumocystis carinii pneumonia (PCP), or Pneumocystis carinii pneumonia, which is the most common and serious opportunistic infection in immunocompromised patients. PC has three structural forms, namely trophozoites, encysts, and cysts (intracapsular bodies.) PC can be parasitic in a variety of animals, such as rats, dogs, cats, rabbits, sheep, pigs, horses, and monkeys, as well as in healthy humans. It is widely distributed in nature, such as soil and water, etc. The main routes of infection of PCP are airborne and activation of latent state PC in vivo. PC multiplies in the lungs and gradually fills the entire alveolar cavity and causes vacuolation and shedding of alveolar epithelial cells. Alveolar epithelial cells proliferate, and type I epithelial cells may show degenerative changes, cell shedding and alveolar wall necrosis, but no purulent changes. Type II epithelial cells are swollen. The interstitial lung is congested and edematous, with widened alveolar septa. The incubation period of PCP is usually 2 weeks, while that of AIDS patients is about 4 weeks. There are no gender or seasonal differences in the onset of the disease. It is important to note that the clinical manifestations of PCP vary considerably among individuals and in different stages of the disease. It is usually divided into two types according to clinical manifestations. The epidemic or classic type is mainly in premature and malnourished infants, mostly between 2-6 months of age, and can be prevalent in nursery institutions. The onset of the disease is often insidious and progresses slowly. Initially, there is mostly lethargy or loss of appetite, diarrhea, low fever, weight loss, and gradually a dry cough and shortness of breath, with progressive worsening, dyspnea, nasal flapping and cyanosis. Sometimes splenomegaly may occur. The course of the disease usually lasts 3-8 weeks, if not treated in time, it can die of respiratory failure, and the death rate is 2O%-50%. 2, disseminated or modern type Most often seen in immunodeficient people, occasionally seen in healthy people. PCP progresses rapidly in patients with chemotherapy or organ transplantation, while it progresses more slowly in patients with AIDS. Initial manifestations include loss of appetite and weight loss. This is followed by dry cough, fever, fever group, respiratory distress, and soon respiratory distress, with a mortality rate of 70%-100% in patients not detected and treated in time. Patients with PCP often show a separation of symptoms and signs, i.e., although the symptoms are severe, the signs are often absent. A small number of patients may have several relapses, which are more common especially in patients with AIDS. The peripheral blood leukocytes are elevated and in some patients reduced, with normal or left-shifted nuclei, increased eosinophils, and decreased absolute lymphocytes. Arterial blood gas analysis shows hypoxemia and respiratory alkalosis. Lactate dehydrogenase was significantly elevated. Pulmonary function tidal volume, total lung volume and diffusion volume are reduced. Early typical changes on chest x-ray are diffuse bilateral perihilar exudates with reticular and small nodular shadows, which then rapidly progress to butterfly shadows in the bilateral hilum, showing pulmonary solidity and visible bronchial inflation signs. Citrate 67Ga, technetium diethylenetriamine ethtalate (99mTc DTPA), and polyclonal immunoglobulin 111ln imaging show abnormalities and therefore can be used as a diagnostic screen for PCP, but with poor specificity. Pathogenic examination can be performed with sputum or induced sputum specimens, fiberoptic bronchoscopic brushings, transbronchial lung biopsies, bronchoalveolar lavage, percutaneous lung puncture and open lung biopsies to stain specimens to observe the capsule wall, intracapsular structures and trophozoites. The use of gene amplification techniques can significantly improve the sensitivity and specificity of diagnosis compared to conventional staining methods. In addition to symptomatic treatment and treatment of the underlying disease, the main focus is on pathogenic treatment. Compounded sulfamethoxazole, aminophenyl sulfone, pentamidine hydroxyethyl sulfonate and trimethoprim trimethoprim are available. Echinocandins antifungal agents such as caspofungin are also effective in PCP.