Black crusts on the palate are commonly associated with pulmonary trichinosis. Pulmonary trichomycosis is an infectious disease of the lungs caused by pathogenic bacteria of the order Trichophyton. Although rare, it develops rapidly and has a high mortality rate. Clinically, Trichoderma and Rhizopus are more common, the former mainly invades the lungs, the latter mostly involves the sinuses, eyes, brain and gastrointestinal tract, and can be hematogenously disseminated to the whole body. Pulmonary trichinosis can be a primary infection, but also secondary to sinus lesions or trichinosis sepsis. The disease begins as a symptom of acute bronchitis, and when the lungs are involved, it causes pulmonary solids and lung abscesses with signs of thrombosis and infarction. So what is the pathogenesis of black crust on the palate? Here we will take a look. In the normal human body, human plasma has the function of inhibiting the growth of Rhizopus spp. and neutrophils have the function of killing mycelium. When the body’s defense mechanism is destroyed or weakened, pathogenic bacteria can invade the body. The respiratory tract is the main route of infection, but also through the skin and intestinal tract. Diabetic acidosis, hematological diseases, lymphoma, myelodysplasia, long-term application of adrenocorticotropic hormones, chemotherapy and radiotherapy are the causative factors of Trichoderma infection, of which severe leukopenia and diabetes are very important. The pathogenic bacteria grow and multiply from the nasal mucosa and submucosa tissues, and soon destroy the tissues causing sinusitis, periocular tissue inflammation, and can also directly invade the brain and meninges, or lungs. Spores that invade the lungs can cross the bronchial walls into the lung tissue and blood vessels and grow rapidly in the tissue. Small arterial vascular embolism and acute purulent inflammation of the lung parenchyma with massive leukocyte infiltration and tissue necrosis. Mycelium invades the blood vessels and causes embolism, which not only accelerates the spread of infection, but also causes tissue infarction. Pathological changes are mainly manifested by vascular embolism and tissue necrosis.