PubMedDate not supplied
Presentation of bronchial asthma, in the years following the first outbreak of bronchiolitis due to respiratory syncytial virus (RSV) was first described by McIntosh, who postulated a common pathogenesis that was confirmed by the greater frequency (50%) of wheezing bronchiolitis and asthma during the more than 5 year follow up of these children. More recently, Hibbert and Schroechkenstein have again confirmed this phenomenon. These authors report that the percentage of asthma was increased by up to 71% in a group of children who contracted bronchiolitis during the first year of life and who were closely followed-up for 5 years after the outbreak. Other authors report figures between 25% and 57%. Stein et al. followed-up 888 children with RSV bronchiolitis until the age of 13 years and observed that at the age of 3-5 years 69% had asthma, at 4-5 years 55% did so and at 6-8 years 31% were asthmatic. In our experience of children who developed RSV bronchiolitis before the age of 6 months, 58 of 75 developed infantile asthma in following 3 years. Seventeen infants were aged more than 6 months at onset of bronchiolitis and of these 5 had bronchiolitis. We carried out a prospective study of 50 children aged 3-7 months with RSV bronchiolitis from December 1997 to February 1998. Follow-up was until the year 2000. Of these children, 22 (44%) had asthma and the remaining 28 (56%) had isolated episodes of cough and wheezing, which did not fulfill the criteria for asthma. Of the 22 children with asthma, all presented elevated total IgE by the second year of follow-up but only one of the children presented hypersensitivity to egg. The breathing difficulties that appeared in the initial outbreak of bronchiolitis is well explained by the cytopathic effect of the virus on the airways of infants. RSV virus produces inflammation of the bronchial mucosa, the effects of which may persist for 6-7 weeks, even after recovery from the first episode. The damaged and denuded epithelium provides fertile ground for future viral reinfections which, although less severe, produce dyspnea due to irritation of the exposed vagal receptors. Irrespective of the mechanism involved (RSV, histamine, methacholine or ozone inhalation) inflammation alters the intercellular junctions of the bronchial mucosal epithelium which, even in the absence of significant necrotic lesions, leads to increased penetration of irritants and stimulates the vagal receptors, leading to bronchospasm. In conclusion, it can currently be stated that RSV bronchiolitis constitutes a risk factor for the development of infantile asthma. The risk is increased in children with familial or personal antecedents of atopy. Serious forms of bronchiolitis due to RSV are more frequent in atopic individuals. The appearance of extrinsic asthma is more frequent in children who have previously had RSV bronchiolitis than in those who have not.