SYNOPSIS The pathological changes are described in 22 children with proven or suspected virus infection of the lower respiratory tract. Two main patterns of disease were found: acute bronchiolitis and interstitial pneumonia. Particular viruses were not specifically associated with particular histological changes. The prime importance of the respiratory syncytial virus (RSV) as a cause of disease and death in young infants is again shown. Structural lesions and clinical dysfunction correlate fairly well; in acute bronchiolitis the main lesion is epithelial necrosis when a dense plug is formed in the bronchiolar lumen leading to trapping air and other mechanical interference with ventilation: in interstitial pneumonia there is widespread inflammation and necrosis of lung parenchyma, and severe lesions of the bronchial and bronchiolar mucosa as well. The implications of these structural changes for clinical management are discussed. The possibility of a hypersensitivity reaction in the cot death syndrome is raised, mediated by a serum antibody-antigen-complement reaction.In 1967 3,000 children died in England and Wales from infection of the respiratory tract. They accounted for 27 % of all deaths in children between the ages of 1 month and 15 years. Seventy-five per cent were infants under the age of 1 year, and 46 % died at home (General Register Office, 1967, and personal communication). The corresponding figures for our community, the northern region of England, were 204 deaths of which 80 % were infants. In Newcastle, of every 100 acute infective illnesses in the first five years oflife, 60 affect the respiratory tract, and 17 are either bronchitis, bronchiolitis, or pneumonia. A large and challenging task, therefore, still faces those concerned with the clinical management of these illnesses and a clearer understanding of their aetiology and pathogenesis is urgently needed.Except in proven bacterial infections aetiology

11 the severity of the clinical symptoms could not be adequately explained by valvular regurgitation, of which there was little evidence on examination of the heart. Blood cultures usually remained sterile, presumably because of inappropriate antibiotic treatment or the limited infectiveness of the organisms present, or both.A striking feature in three patients (cases 1, 2, and 4) was the acute, severe, and rapidly resolving but recurrent episodes of pulmonary oedema. Possibly these were caused by sudden blocking of the orifice by -vegetation-this was indeed shown echocardiographically in one patient (case 4). Other patients (cases 3 and 5 and those reported by Reeve et all and Matula et al2) had more progressive pulmonary oedema, suggesting increasing mitral stenosis. In our experience both types of pulmonary oedema are uncommon in patients with isolated mitral valve regurgitation during bacterial endocarditis.Those of our patients who did not have mitral valve replacement (cases 2, 4, and 5) and the patient of Reeve and his colleagues' had a sudden cardiac arrest. Mitral valve vegetations cause obstruction just as catastrophic as an atrial tumour or a ball thrombus, and hence once the doctor suspects mitral valve obstruction he should confirm the diagnosis promptly and ensure that the patient is rapidly operated on.Accurate diagnosis is vital. Right heart catheterisation showed a raised pulmonary wedge pressure without a striking V wave, but was nevertheless of little value in assessing the severity of the haemodynamic disturbance: pressures may be very high because of rheumatic valve disease (case 4) Journal, 1978, 1, 11-14 Summary and conclusions Thirty-five children known to have had respiratory syncytial virus bronchiolitis in infancy were examined at the age of 8 and their respiratory function tested. The results were compared with those in 35 controls matched for age, sex, and social class. Although 18 of the children who had had bronchiolitis in infancy had experienced subsequent episodes of wheezing, these were neither severe nor frequent in most cases and had apparently ceased by the age of 8. Nevertheless, the mean exercise bronchial lability of the children who had had bronchiolitis was significantly higher than that of the control children and the mean peak expiratory flow rate at rest significantly lower.

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