What is the pathophysiology of pneumonia in infants and young children?

Pathophysiology of Pediatric Pneumonia

Pediatric pneumonia results from infection of the lung parenchyma by pathogens that vary predictably by age, with younger children predominantly affected by viral invasion of small airways causing obstruction and atelectasis, while older children experience bacterial alveolar consolidation, most commonly from Streptococcus pneumoniae. 1, 2

Age-Dependent Pathophysiologic Mechanisms

Infants and Young Children (<5 years)

The peripheral airways of infants are anatomically more susceptible to inflammatory narrowing than adults, making small airway obstruction the primary pathophysiologic mechanism rather than alveolar consolidation. 3

• Viral pathogens (14-35% of cases) cause bronchiolar inflammation leading to airway obstruction, air-trapping, and atelectasis rather than true consolidative pneumonia. 1, 3
• Respiratory syncytial virus (RSV) is the predominant viral pathogen, causing bronchiolar epithelial damage and mucus plugging. 1
• The resulting airway obstruction manifests radiographically as generalized hyperinflation and irregular aeration patterns. 3
• This small airway obstruction frequently causes severe respiratory embarrassment disproportionate to the degree of parenchymal involvement. 3

School-Aged Children and Adolescents (≥5 years)

Older children develop classic bacterial pneumonia with alveolar consolidation, following a pathophysiologic pattern more similar to adults. 1

• Streptococcus pneumoniae (16-37% when serologic testing is used) causes alveolar filling with inflammatory exudate and consolidation. 1
• Mycoplasma pneumoniae (4-39% of cases) and Chlamydia pneumoniae (0-20%) cause interstitial inflammation with a slowly progressive course over 3-5 days. 1, 4
• These atypical pathogens produce less severe alveolar consolidation with more prominent interstitial involvement. 4

Pathogen-Specific Mechanisms

Bacterial Pneumonia

Streptococcus pneumoniae remains the most common bacterial cause across all pediatric age groups, causing acute alveolar inflammation and consolidation. 1, 2

• Pneumococcal invasion triggers acute inflammatory response with neutrophil recruitment and alveolar exudate formation. 1
• Staphylococcus aureus (particularly in infants <6 months) causes necrotizing pneumonia with tissue destruction and frequent ICU admission. 1, 2
• Haemophilus influenzae type b is now rare in appropriately immunized children. 2

Atypical Bacterial Pneumonia

Mycoplasma pneumoniae causes slowly progressive interstitial inflammation beginning with upper respiratory symptoms before descending to the lower airways. 4, 5

• The pathophysiology involves attachment to respiratory epithelium without tissue invasion, causing ciliary dysfunction and inflammatory response. 4, 5
• This produces the characteristic slowly progressive illness over 3-5 days with malaise, sore throat, low-grade fever, and eventually cough. 4
• Wheezing occurs in approximately 30% of cases due to bronchial inflammation and hyperreactivity. 4, 5

Viral Pneumonia

Viral pathogens cause direct epithelial cell damage and inflammatory response in bronchioles and alveoli, with RSV being the predominant pathogen in young children. 1

• Viral invasion causes epithelial necrosis, increased mucus production, and bronchiolar obstruction. 3
• Secondary bacterial infection occurs in 8-40% of cases, representing mixed viral-bacterial pathophysiology. 1, 2

Mixed Infections

A significant proportion (8-40%) of pediatric pneumonia cases involve co-infection with multiple pathogens, complicating the pathophysiologic picture. 1, 2

• Mixed viral-bacterial infections occur in 30% of cases, with dual viral infections in 13% and dual bacterial infections in 7%. 1
• Co-infection typically involves viral disruption of epithelial barriers facilitating secondary bacterial invasion. 1

Clinical Implications of Pathophysiology

Severity Determinants

Young age (<6 months) is an independent risk factor for severe disease due to anatomically smaller airways and immature immune responses. 1

• Attack rates are highest in infants (35-40 per 1000) compared to school-aged children (15 per 1000). 1
• Infants have greater risk of respiratory failure requiring mechanical ventilation due to small airway obstruction. 1, 3

Complications

The pathophysiology can progress to necrotizing pneumonia (particularly with CA-MRSA), pleural effusion/empyema, or respiratory failure requiring ICU admission. 1

• Panton-Valentine leukocidin-positive S. aureus causes tissue necrosis with 78% requiring mechanical ventilation. 1
• Impending respiratory failure manifests as sustained tachycardia, inadequate blood pressure, or oxygen saturation ≤92% on FiO2 ≥0.50. 1