One hundred newborn infants were studied prospectively for 1 year for evidence of infection with respiratory syncytial virus (RSV). The indirect membrane fluorescence technique was used to determine specific antibody in sera. Infection was shown in 29 cases. In 31 infants exposed to an RSV epidemic season, there was no evidence of infection. Maternal antenatal sera were also tested, and wide range of IgG antibody to RSV was found. Mean titre of maternal IgG antibody to RSV was significantly higher (P less than 0.001) in those mothers whose babies remained uninfected than in those whose babies had proved RSV infection before 6 months of age. Babies born to mothers with high levels of IgG antibody to respiratory syncytial virus were protected against infection with this virus during the first months of life when the risk of severe disease was greatest.

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The time course of change in FEV1, bronchial reactivity, and daily measures of asthma control (peak expiratory flow, symptoms, and beta 2-agonist inhaler use) was determined during 6 wk of treatment with inhaled budesonide, 800 micrograms twice a day, and for 2 wk following cessation of treatment in 40 asthmatic subjects in a double-blind, placebo-controlled, parallel group study. Histamine reactivity, expressed as the provocative dose of histamine causing a 20% fall in FEV1 (PD20), was measured at intervals during the 8 wk of the study, with more frequent measurements after the first and last dose of drug to provide a detailed profile of change at the start and end of treatment. The first dose of budesonide caused a small increase in median values of FEV1 (0.2 L) and PD20 (1.0 doubling dose of histamine), which was maximum at 6 h. There was a further increase in FEV1 and PD20 over the 6 wk in the budesonide group relative to placebo, the maximum increases (0.53 L, 3.4 doubling doses of histamine) being recorded 6 h after the last dose on Day 42. Following cessation of treatment, FEV1 and PD20 declined and PD20 returned to placebo values at 1 wk. Median PEF increased by 40 and 30 L/min in the morning and evening, respectively, with budesonide treatment. Symptom scores and beta 2-agonist inhaler use were lower in the budesonide group than the placebo group during treatment but tended to be similar (symptom scores) or higher (beta 2-agonist) in the 2 wk following cessation of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

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Background It has been suggested that inhaled corticosteroids may provide greater protection against constrictor stimuli that act indirectly such as exercise than those that act directly such as histamine. Methods The effects of six weeks treatment with inhaled budesonide (800 ug twice daily) on bronchial reactivity to histamine, exercise, and eucapnic voluntary hyperventilation of dry air were compared in a double blind, placebo controlled, non-crossover study in 40 subjects with asthma. Change in bronchial reactivity to histamine and eucapnic hyperventilation over the six weeks was measured as change in the provocative dose of histamine or dry air causing a 20% fall in FEV, (PD20 histamine and PV20 eucapnic hyperventilation (EVH) of dry air); this was not possible for exercise because of the development of refractoriness. To enable the change in response to all three stimuli to be compared, the response (percent fall in FEV,) to a fixed dose was measured for all three challenge tests. Results After budesonide there was an increase in PD20 histamine from 0-48 to 2-81 pmol and in PV20 EVH from 364 to 639 litres, and a significant correlation between the changes in PD20 histamine and PV20 EVH (r = 0-63). The median percentage fall in FEV, in response to eucapnic hyperventilation, exercise, and histamine was similar before budesonide (25-5%, 26-6%, and 24-5%); the reduction in the percentage fall in FEV, with budesonide was also similar for the three challenges (18-9%, 17-5%, and 16-6%), and all differed significantly from the changes following placebo. There was a significant correlation between change in percentage fall in FEV, after budesonide with the three stimuli (histamine v exercise: r = 0-48; histamine v eucapnic hyperventilation: r = 0-46; exercise v eucapnic hyperventilation: r = 0-63). Conclusion The similar magnitude of change in bronchial reactivity to all three stimuli after budesonide and the within subject correlation obtained between these changes suggest that corticosteroids act by a common mechanism to protect against eucapnic hyperventilation, exercise, and histamine.Patients with asthma show increased airway reactivity to a wide range of stimuli, some of which appear to act directly on airway smooth muscle and some indirectly through mast cell mediator release or sensory nerve stimulation. Drugs such as beta2 agonists reduce bronchial reactivity irrespective of the stimulus, whereas others, such as sodium cromoglycate and inhaled frusemide, reduce the airway response to challenges that act indirectly, such as exercise,' 2metabisulphite,3'4 and cold air hyperventilation,5 with little or no effect on directly acting stimuli such as histamine and methacholine.67Corticosteroids when given regularly have been shown to inhibit the response to most bronchoconstrictor stimuli,"'9 but whether they give similar protection against different forms of challenges is not clear. It has been suggested that they may have a greater effect on exercise induced bronchoconstriction than that induced by hist...