Etiology
The most common cause is respiratory syncytial virus (RSV). One meta-analysis of studies examining respiratory viruses found in children under 2 years of age with bronchiolitis confirmed that RSV predominated (59.2%, 95% CI 54.7 to 63.6), while rhinovirus was second most common (19.3%, 95% CI 16.7 to 22.0). Human bocavirus accounted for 8.2% (95% CI 5.7 to 11.2), adenovirus was found in 6.1% (95% CI 4.4 to 8.0), human metapneumovirus occurred in 5.4% (95% CI 4.4 to 6.4), parainfluenza was detected in 5.4% (95% CI 3.8 to 7.3), influenza in 3.2% (95% CI 2.2 to 4.3), coronavirus in 2.9% (95% CI 2.0 to 4.0), and enterovirus in 2.9% (95% CI 1.6 to 4.5). In those babies with multiple viruses detected, RSV was most commonly found with rhinovirus or human bocavirus.[14][15] In a 2023 study looking at severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) bronchiolitis, in 2004 infants diagnosed with bronchiolitis, 95 (4.7%) were tested positive for SARS-CoV-2.[12]
Bronchiolitis caused by RSV and other respiratory viruses begins as an upper respiratory tract infection, which then spreads to the lower respiratory tract in 1 to 3 days.
RSV infection occurs in almost all infants by age 2 years, but only a minority develop bronchiolitis. This observation has led to the hypothesis that host and possibly environmental factors play a role in disease pathogenesis.[16] Birth cohort studies have shown that diminished lung function at birth is a risk factor for wheezing in early infancy, but this mechanism cannot completely explain the variability of clinical manifestations of RSV infection.[17][18]
Environmental tobacco smoke exposure may contribute to disease severity.[19][20][21] Similarly, environmental pollutants are linked to more severe RSV disease. A time-series study from northwestern Italy reported an association between the concentration of 10-micron airborne particulate matter (PM10) with rates of RSV hospitalization in infants under 1 year of age; PM10 concentrations in the 2 weeks preceding hospital admission were strongly associated with an increased risk of RSV hospitalization.[22] The authors speculated that environmental factors such as air pollution could affect an infant's immune system and limit responses to viral illnesses.
Another area of focus has been the role of the host immune response in determining the effects of RSV infection.[23]
Pathophysiology
The virus infects the respiratory epithelial cells of the small airways, leading to necrosis, inflammation, edema, and mucus secretion. Neutrophils are the predominant inflammatory cells that invade the airways in severe RSV disease. The combination of cellular destruction and inflammation leads to obstruction of the small airways. The physiologic and clinical results consist of hyperinflation, atelectasis, and wheezing. In severe cases, interstitial inflammation and alveolar infiltrates also develop. Regrowth of the epithelial cell layer does not occur until approximately 2 weeks after infection, with complete recovery requiring 4 to 8 weeks.
Early studies reported that RSV infection was associated with mediators typically produced by type-2 helper T cells (TH2 cells).[24][25][26][27] However, subsequent clinical studies have suggested that the severity of RSV infection and the likelihood of wheezing with any respiratory viral infection probably reflects alterations in the infant's innate and adaptive immune responses to infection.[28][29][30][31][32] Additionally, RSV may inhibit the lung antioxidant system and promote the development of reactive oxygen species, resulting in increased lung oxidative damage.[33]
Classification
Clinical entities of bronchiolitis
RSV bronchiolitis
Viral bronchiolitis caused by RSV
Non-RSV bronchiolitis
Viral bronchiolitis cases in which RSV has not been detected
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