Respiratory syncytial virus (RSV) causes 50 to 70 percent of clinically significant bronchiolitis. 37 First isolated in the 1950s, it is a significant cause of infant morbidity and is one of the major causes of hospital admission in infants below 1 year of age. Symptoms can vary from minimal rhinorrhea to bronchiolitis or pneumonia. Of the two antigenic subtypes of RSV, A and B, the former is generally more severe but less common. Two surface proteins, G (attachment) and F (fusion), are necessary for RSV to cause infection. Research is concentrating on F protein antibodies, which show less antigenic diversity than G proteins and neutralize both RSV subtypes. Immunity to the virus is variable owing to antigenic diversity; therefore reinfection does occur. No vaccine has yet been identified.

Non-RSV bronchiolitis is caused by influenza virus, parinfluenza virus, echovirus, and rhinovirus. Mycoplasma pneumoniae and Chlamydia trachomatis also produce symptoms. Adenovirus causes a particularly destructive form, bronchiolitis obliterans, observed in Native Canadian Eskimo populations.

Mucous plugging results from necrosis of the respiratory epithelium and destruction of ciliated epithelial cells. This and submucosal edema lead to peripheral airway narrowing and variable obstruction, with areas of patchy atelectasis or overdistention in lung segments. Progressive disease causes severe pneumonia, with extensive destruction of respiratory epithelium, parenchymal necrosis, and formation of hyaline membranes. Bronchiolar regeneration occurs within 3 to 4 days; however, cilia may take as long as 15 days to regenerate.

Increased airway resistance and decreased compliance result in increased work of breathing. Like the infant with lower airway obstruction, the infant with bronchiolitis breathes at higher lung volumes due to uneven resistance within the lung. Alteration of gas exchange results from the patchy atelectasis and airway obstruction. V/Q mismatch is variable and severe hypoxemia may result.

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