Lobar pneumonia is an inflammatory disease mainly caused by Streptococcus pneumoniae with diffuse intra-alveolar fibrinous exudate, usually involving all or most of the large lobes of the lung. The disease is usually seen in young adults and has a rapid clinical onset, with the main symptoms being chills, high fever, cough, chest pain, dyspnea and coughing up rust-colored sputum, signs of solid lung changes and peripheral blood leukocytosis. The symptoms and signs usually subside after 5-10 days when the body temperature decreases. Etiology and pathogenesis: More than 90% of lobar pneumonia is caused by Streptococcus pneumoniae, of which types 1, 3, 7 and 2 are common, but type 3 is the most virulent. In addition, Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, and Streptococcus haemolyticus can also cause it, but all are rare. Streptococcus pneumoniae is present in the nasopharynx of normal people, and normal people with the bacteria are often the source of transmission of the disease. Pathologic changes and clinicopathologic associations: The main pathologic change in lobar pneumonia is fibrinitis in the alveolar cavity, which often occurs in the unilateral lung, mostly in the left or right lower lobe of the lung, but can also occur in two or more lobes simultaneously or sequentially. The typical natural pathogenesis can be roughly divided into four phases: 1. Congestive edema phase: On the first 1-2 days of the disease, the diseased lung lobes are swollen and dark red. Microscopically, the alveolar septum is seen to be diffusely dilated and congested with capillaries, and there is a large amount of plasma exudate in the alveolar cavity, which is mixed with a small amount of red blood cells, neutrophils and macrophages. Streptococcus pneumoniae can often be detected in the exudate. Patients in this stage have chills, high fever and elevated peripheral blood leukocyte counts due to toxemia. Chest x-ray shows faint shadows in a lamellar distribution. 2. Red hepatomegaly stage: It usually occurs on the 3rd-4th day after the disease, the enlarged lung lobes are congested with dark red, solid texture and gray-red cut surface, resembling the appearance of liver, so it is called red hepatomegaly stage. Microscopically, the capillaries in the alveolar septum were still dilated and congested, while the alveolar cavity was filled with fibrin and a large number of red blood cells, interspersed with a small number of neutrophils and macrophages. The fibrin filaments were connected into a network and passed through the alveolar interstitial pores to connect with the fibrin network in the adjacent alveoli. Streptococcus pneumoniae can still be detected in large amounts in the exudate at this stage, and a large dense shadow can be seen on x-ray. If the lesion is widespread, the partial pressure of oxygen in the arterial blood of the patient decreases due to alveolar ventilation and alveolar ventilation dysfunction, and cyanosis and other symptoms of hypoxia may occur. When the lesion spreads to the pleura, it causes fibrinous pleurisy and chest pain, which can be aggravated by breathing and coughing. 3, gray liver-like changes: the 5th-6th day after the onset of the disease, the lesion lung lobes are still enlarged, but the congestion subsided, from red gradually changed to gray-white, solid texture such as liver, so called gray liver-like changes, microscopically seen in the alveolar cavity exuding more fibrin, adjacent alveolar fibrin filaments through the inter-alveolar pore interconnected phenomenon is more common, fibrin network with a large number of neutrophils, because the alveolar wall capillary compression, alveolar cavity The red blood cells are rarely seen in the alveolar cavity because of the compression of the alveolar wall capillaries. At this stage, although the alveoli still cannot be inflated, the amount of blood filling in the diseased lung tissue is significantly reduced due to the compression of the alveolar interstitial capillaries, so that the venous oxygen deficiency is reduced instead, and therefore the hypoxic condition improves. The other clinical symptoms of the patient began to decrease, and the rust-colored sputum coughing up gradually changed to mucus-colored sputum. In addition to the germs in the exudate being killed by neutrophil phagocytosis, the specific antibodies of the body have been formed at this time, so it is not easy to detect the bacteria. 4, dissolution dissipation period: about 1 week after the onset of the disease into the period. At this time, the body’s defense function is significantly enhanced, the germs are eliminated. Neutrophils in the alveolar cavity become degenerative and necrotic, and a large amount of proteolytic enzymes are released to dissolve the fibrin in the exudate, which is absorbed by the lymphatic vessels or cough up through the airways. Solid lesions within the lungs disappear and the diseased lung tissue is soft in texture. After complete dissolution and dissipation of the inflammatory lesions in the lungs, the lung tissue structure and function return to normal, and the pleural exudate is absorbed or mechanized. The patient’s body temperature decreases, clinical symptoms and signs gradually decrease and disappear, or the chest X-ray examination returns to normal. This period lasts about 1-3 weeks.