Both lungs are continuously exposed to particles and microorganisms, which appear in the upper respiratory tract and then enter the lower respiratory tract by microaspiration. Nevertheless, the lower respiratory tract is usually sterile due to the defensive mechanism of the lungs. These host defenses can be classified into congenital (non-specific) and acquired (specific). The occurrence of CAP suggests the defect of host defense, exposure to particularly virulent microorganisms or colonization of a large number of bacteria.
Although microaspiration is the most common pathogenesis that causes pathogens to reach the lungs, other pathogenesis also includes the spread of blood from distant infection sites, the direct spread of adjacent lesions and a large number of aspiration errors.
Toxicity factors - Some microorganisms have developed specific mechanisms to break down host lung defenses and cause infection. For example:
Chlamydia pneumoniae can produce factors that inhibit ciliary movement.
Mycoplasma pneumoniae can cut off cilia.
Influenza viruses can significantly reduce the tracheal mucus clearance rate within hours of infection and last up to 12 weeks after infection.
Streptococcus pneumoniae and Neisseria meningitidis can produce proteases capable of lysing secretory immunoglobulin (Ig) A. In addition, pneumococcus produces other virulence factors, including the capsule that inhibits phagocytosis, Streptococcus pneumoniae hemolysin (thiol-activated cytolysin interacting with cholesterol on the host cell membrane), neuraminidase and hyaluronidase.
Some species of Mycobacterium, Nocardia and Legionella can resist the bactericidal activity of phagocytes.
Physical condition of susceptible hosts - In addition to virulence factors of microorganisms, host diseases and physical conditions may lead to impaired lung defense and increased risk of CAP. These include:
Changes in the level of consciousness [susceptible to massive aspiration of gastric contents (caused by stroke, epilepsy, drug p
