Etiology

The true prevalence of different etiologic pathogens in childhood CAP is difficult to determine because many affected children do not undergo microbiologic tests and, in those who do, it is common to identify either no specific etiologic agent or mixed infections.

Viral pathogens have become increasingly predominant since the routine introduction of vaccinations against Streptococcus pneumoniae and Haemophilus influenzae b (Hib).[1][8]​ A US multicenter study that reported etiologic data for 2222 children who required hospitalization for CAP between 2010 and 2012 detected a viral pathogen in 73% and a bacterial pathogen in 15%. Multiple pathogens were detected in 26% of the children.[4]

The proportion of different etiologic agents varies by age group. Viruses have been reported to account for up to 80% of all cases in children <2 years old and to account for 30% to 67% of hospitalized cases in all preschool-age children.[1]​​[3][4]​​ Respiratory syncytial virus (RSV) is the most common etiology, accounting for up to 40% of identified pathogens in children <2 years old and around one quarter in the 2-4 years age group, but is less commonly reported in older children.[1]​​[3][4]​ Other common viral pathogens include rhinovirus, adenovirus parainfluenza, influenza, and human metapneumovirus.​[3][4]​​[7]​​[9]

In school-age children and young adolescents, bacterial pneumonia is more common than in infants and preschool children, although viral etiologies still predominate.[4][10]​  S pneumoniae is the most common typical bacterial pathogen, accounting for 4% of detected pathogens in 5- to 17-year-olds hospitalized with CAP in the US, although atypical infection with Mycoplasma pneumoniae is a more frequent bacterial cause of CAP (22% of detected pathogens in the 5-17 years age group).[4][10]

Mixed viral-bacterial coinfection is common, with evidence suggesting it is present in up to one third of cases.[1][9]

Pathophysiology

​CAP develops subsequent to the invasion of the lower respiratory tract by pathogens. Infectious agents, inhaled or aspirated directly into the lungs, may spread to the respiratory epithelium and, less frequently, reach the lungs hematogenously.[4]

Viral inoculation occurs by droplets or fomites (e.g., influenza, respiratory syncytial virus), which travel to the lower respiratory tract, multiply, and cause de-epithelialization and ciliary dysfunction, resulting in mucus plugging and fibrosis of the airways and consequently air trapping and hyperinflation. Once the virus spreads to the alveoli, surfactant synthesis is affected, and hyaline membranes and pulmonary edema can appear.[11]​ All these events can cause segmental or subsegmental atelectasis and increase ventilation-perfusion mismatch and hypoxemia. Lastly, by infiltrating the submucosal and interstitial spaces, mononuclear cells worsen edema and further affect gas exchange across alveolar membranes.[11]

Bacterial CAP occurs as a result of colonization of the nasopharynx, after which bacterial agents spread into the respiratory epithelium, resulting in interstitial inflammation and alveolar injury.[11] The air space fills with mononuclear cell infiltrate and exudate, affecting oxygenation and resulting in a ventilation-perfusion mismatch. Exudative fluid allows the bacteria to multiply and spread to adjacent alveoli, contributing to the typical pattern of lobar pneumonia.[12]

There are four stages of lobar pneumonia:[4][11][12]

  • The first stage occurs within 24 hours and is characterized by alveolar edema and vascular congestion. Bacteria and neutrophilic infiltrates can be present.

  • The second stage, also known as red hepatization, is characterized by neutrophils, red blood cells, and desquamated epithelial cells. Fibrin deposits in the alveoli are common.[12]

  • The third stage, called gray hepatization, occurs 2-3 days later and is typified by hemosiderin and hemolysis of red cells, resulting in a dark brown aspect of the lung.[12]

  • The last stage is the resolution stage, characterized by reabsorption of cellular infiltrates and restoration of the pulmonary architecture. If optimal healing fails to take place, parapneumonic effusions and pleural adhesions can develop.[12]

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