Pathophysiology

The majority of pneumonias are acquired through aspiration of infective particles into the lower respiratory tract. There are a number of protective mechanisms preventing infection with aerosolized infective particles. Aerosolized particles are filtered in the nasal cavities or entrapped and cleared by the normal mucus and ciliated epithelium of the upper respiratory tract. Aspiration is further prevented by laryngeal reflexes and coughing. In the lower respiratory tract, alveolar macrophages and various immune mechanisms prevent further invasion by infectious agents. These defense mechanisms include the ingestion and killing of bacteria by macrophages, the activation of complement and antibodies that neutralize bacteria, and the transportation of particles from the lung by lymphatic drainage. Abnormalities in any of these protective mechanisms predispose patients to acquired pneumonia. Anatomic abnormalities of the respiratory tract, immune deficiencies, neuromuscular weakness, airway abnormalities that predispose the child to aspiration, and alterations in the quantity or quality of mucus secretion (e.g., cystic fibrosis). Passively acquired maternal antibodies may further prevent respiratory tract infection by pneumococcal and Haemophilus influenzae infections.

Suppression of the normal respiratory physiologic and anatomic defenses may occur secondary to a preceding viral infection of the upper respiratory tract. Coexistence of viral and bacterial pathogens in children has been demonstrated in 50 percent or more of cases. 45 Bacteria that cause pneumonia include many of the same organisms that colonize the child's upper airway. In addition, organisms that are transmitted person-to-person by airborne droplet spread may cause pneumonia. Less commonly, bacterial and certain viral (e.g., herpes simplex virus, varicella, rubella, rubeola, and Epstein-Barr virus) microbes may cause pneumonia through hematogenous or contiguous spread.

Parenchymal invasion by bacteria results in an acute inflammatory response that includes exudation of fluid; deposition of fibrin; and infiltration of the alveoli with fluids, polymorphonuclear leukocytes, and, soon, macrophages. Accumulation of excess alveolar fluid creates the characteristic consolidation seen on chest radiograms. Viral agents, mycoplasma, and chlamydia typically cause inflammation characterized by a predominately mononuclear infiltrate involving submucosal and interstitial tissues.

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