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Previous studies from several laboratories have established that adenovirus is a common cause of severe childhood bronchiolitis. The observation that children with an established history of bronchiolitis subsequently developed unremitting airways obstruction even after adequate steroid therapy led us to postulate that this bronchial obstruction might be due to persistence of an adenoviral infection. This hypothesis was tested by performing bronchoalveolar lavage (BAL) on a group of 34 children with a mean age of 5 yr (range, 14 mo to 14 yr) who showed an unfavorable response to standard corticosteroid and bronchodilator therapy. Analysis of cytospin preparations of BAL fluid at the light-microscopic level, using a monoclonal antibody to detect adenoviral antigens, demonstrated that capsid protein was present in 31 of 34 (94%) of the children examined. Limited repeat studies within 1 yr showed 6 of 8 (75%) were positive twice when tested on two occasions, and that three were positive in all occasions when sampled three times. Cultures of the BAL fluid were also positive for adenovirus in six of six cultures performed, indicating that the virus was in some cases replicating. Similar studies of control patients without persistent asthma showed no evidence of adenovirus. We conclude that persistent and/or latent adenoviral infection may contribute to the pathogenesis of childhood asthma in which there is an unfavorable response to steroid and bronchodilatation therapy.

The idiopathic (BOOP) and secondary forms of proliferative bronchiolitis have similar radiographic appearances. Both are characterized radiographically by patchy airspace disease, which often is peripheral. The radiographic presentation of BOOP may have prognostic significance. In primary or secondary constrictive bronchiolitis, the chest radiograph often is nonspecific, but the CT appearance of patchy, lobular areas of hyperlucency, with or without bronchiectasis, may be diagnostic. Respiratory bronchiolitis usually can be distinguished from IPF on the chest radiograph, and the diagnosis may be suggested on HRCT by the presence of hazy increase in lung density or fine centrilobular nodules.

Respiratory syncitial virus (RSV) is a common cause of upper and lower respiratory tract infection in infants. An association between RSV bronchiolitis and cardiac arrhythmias has been described but is rare. A further case of an infant with supraventricular tachycardia in association with culture-positive respiratory syncitial virus bronchiolitis is reported. This case prompted a review of the two other cases of arrhythmia associated with RSV infection seen at this institution and a review of all other published cases.

Background: Respiratory syncytial virus (RSV) infection in infancy can induce bronchial reactivity and virus-specific IgE production; these responses may favor the later development of asthma. This retrospective study examines the influences of early and severe forms of bronchiolitis on such an outcome., Population and Methods: The files of 43 infants who had spent 1 to 24 days (mean 7.8 days) in intensive care between 1986-1990 for severe bronchiolitis with apnea and/or hypercapnia and/or hypoxemia were studied. The parents of all these children agreed to answer a standard questionnaire covering perinatal events, gestational age, number and frequency of recurrent episodes of wheezing, personal and familial history of allergy and environmental conditions. 15 of the children were preterm and 12 of them were given respiratory support during the neonatal period; 5 of these patients developed broncho-pulmonary dysplasia. RSV was isolated in 20 of 39 patients., Results: 26 of the 41 surviving patients developed at least 3 episodes of wheezing over periods ranging from 5 to 54 months (mean 27.6 months): 15 of them were admitted at least once for asthma and 17 were given long-term bronchodilators and/or corticosteroids. Of the 8 patients with histories of allergy, 6 developed asthma, as did 7 of the 9 that had been in close contact with other children, and 9 of the 15 patients who had been exposed to tobacco., Conclusions: Not only is the development of asthma associated with risk factors (RSV infection, bronchopulmonary dysplasia, history of allergy, close contact with other children and exposure to tobacco) but the severity of the bronchiolitis per se is also correlated with this risk.

Airway responsiveness to inhaled methacholine was assessed in 18 infants, 4 and 10 months old, following bronchiolitis. Pulmonary function was measured from partial expiratory flow-volume curves generated by the rapid compression technique. Sleeping infants inhaled increasing concentrations of methacholine until maximal expiratory flows at functional residual capacity (VmaxFRC) decreased by 30% or 2.5 mg/mL was inhaled. Airway responsiveness was quantitated by: 1) the threshold concentration (log TC) required to decrease VmaxFRC by 2 standard deviations from baseline; 2) the concentration required to decrease VmaxFRC by 30% (log PC30); and 3) the slope of the dose-response curve between TC and PC30 (log SPC30). At both the first and second evaluation, the bronchiolitic infants had lower baseline VmaxFRC (% pred.) than 24 control infants. In addition, the bronchiolitic infants had heightened airway responsiveness compared to controls, demonstrating lower values for logTC and logPC30 and steeper slopes to their dose-response curves (logSPC30). After accounting for the relationship between airway responsiveness and age, the occurrence of bronchiolitis was found to be a significant independent factor 10 months but not 4 months following bronchiolitis. The bronchiolitic infants did not demonstrate the decline in airway responsiveness with increasing age that occurs in normal infants. We conclude that infants exhibit heightened airway responsiveness following bronchiolitis.

As part of a long term prospective study, 73 children who had been admitted to hospital with viral bronchiolitis as infants, were reviewed 5.5 years later and compared with a carefully matched control group. In the postbronchiolitis group, there was a highly significant increase in respiratory symptoms including wheezing (42.5% v 15.0%, relative risk = 2.8). Although atopy in the family was not significantly increased in the index group, personal atopy was more prevalent. However, personal atopy was not significantly more prevalent in the symptomatic postbronchiolitis, compared with those who were symptom free, and so did not account for the high prevalence of postbronchiolitis wheezing in this cohort. In addition, in a stepwise logistic regressional model, bronchiolitis remained a significant predictor of wheezing after adjusting for potential confounding variables, including atopy. Bronchial responsiveness to histamine was significantly increased in the index group. However, no significant relationship of positive tests to wheezing could be demonstrated, and a high rate of positive responses was noted in the controls.

Bronchiolitis and wheezy bronchitis are frequently associated with viral infection of the respiratory tract in infants. They play an important role in the natural history of chronic obstructive airway disease, not only in children, but also in adults. The risk of early recurrent wheezing and subsequent asthma or chronic bronchitis (with anatomical sequelae such as obliterans bronchiolitis) is significant. The precise pathogenic mechanisms of virus-induced wheezing and its sequelae are not clear. Whether airway hyperreactivity is inherited and airway hyperreactivity is present prior to, or is the result of bronchiolitis is not clear. Nevertheless the evidence for viral trigger of wheezing and long-term pulmonary sequelae must be considered and prevention must be undertaken at the first episode.

We determined the effects of an immediately antecedent viral lower respiratory tract infection (LRI) on the severity of clinical illness, changes in lung function and airway histamine responsiveness produced by a subsequent LRI in 9-12 week old beagle puppies inoculated with canine adenovirus 2, followed in 2 weeks by inoculation with canine parainfluenza 2 virus (CAV2-CP12, n = 7). We compared their acute responses to puppies infected with CP12 alone (n = 5), CAV2 alone (n = 7), and no infection (control, n = 6). Puppies inoculated with either virus alone developed a LRI 3 to 6 days after inoculation which resolved by 12-14 days after inoculation. However, the illness was more severe in the CAV2 group. In the CAV2-CP12 group, CP12 infection following CAV2 infection resulted in a clinical illness nearly comparable to that observed with CAV2 alone. Whereas in control and CP12 puppies, lung resistance (RL) decreased and dynamic lung compliance (Cdyn) increased during the study due to normal growth, RL increased and Cdyn remained unchanged in the CAV2 group. In contrast, RL did not change and Cdyn increased in the CAV2-CP12 group. Airway histamine responsiveness in the CAV2-CP12 group increased during infection with CP12 and was similar to that observed with CAV2 alone. In contrast, infection with CP12 alone produced a small, but non-significant increase in histamine responsiveness. The duration of the increase in histamine responsiveness was not prolonged in the CAV2-CP12 group in comparison to CP12 or CAV2 alone. However, the length of clinical illness was extended in the CAV2-CP12 group in comparison to the other infected groups. These data suggest that an immediately antecedent viral LRI can potentiate the clinical and physiologic effects of a subsequent viral LRI.

Twenty-one children with normal hearts were studied during acute bronchiolitis. Doppler echocardiography showed tricuspid valve regurgitation in 11 patients, many of whom had evidence of raised pulmonary artery systolic pressure. Serial studies in those with severe infection showed that tricuspid regurgitation disappears with clinical improvement.

Viral bronchiolitis in human infants has been associated with permanent changes in small airways and gas exchange and an increased incidence of hyperresponsive airways later in life. Respiratory infection by Sendai virus in neonatal rats also has been reported to cause permanent changes in lung morphology and increased numbers of bronchiolar mast cells and eosinophils. We evaluated pulmonary mechanics, gas exchange, and airway responsiveness in rats at 7 and 13-16 wk after neonatal Sendai virus infection. Rats from the virus group had lower arterial PO2 and increased total lung resistance compared with controls. There were no significant differences between groups for arterial PCO2, dynamic lung compliance, quasi-static respiratory system compliance, or vital capacity. Rats from the infected group were significantly more sensitive to aerosolized methacholine than were controls, although both virus and control groups became less sensitive with age. We conclude that neonatal Sendai virus infection in rats results in persistent alterations in lung function and airway responsiveness. This phenomenon may be valuable for the study of the relationships among airway inflammation, lung morphology, and airway hyperresponsiveness, and it may be relevant to human airway disease.

Between may 1984 and november 1986, a study, which included 475 children under five years of age hospitalized due to acute intrathoracic respiratory infections, was carried out in order to obtain clinical, radiological and etiological characteristics which may aid in establishing norms to diagnose and treat these patients. Nasopharyngeal aspirations were performed on each child, while viral diagnosis was done through viral isolation techniques and indirect immunofluorescence. The presence of a virus was detected in 34.4% of the cases and in 28.8% of a subsample. A precoded questionnaire was used to obtain the clinical information needed and all X-rays were reviewed by the same radiologist using simple pre-established criteria. A comparison was made on the similarities found between both the clinical and radiological diagnosis, as well as the sensitivity and specificity of some of the clinical signs which characterize bronchiolitis and the pneumoniae.

Cytomegalovirus (CMV) is frequently isolated from respiratory secretions of human immunodeficiency virus (HIV)-infected patients. Even in the presence of histopathologic evidence of CMV cytopathic abnormalities, the true clinical significance of CMV pneumonitis is not well established. Airways disease is increasingly recognized in HIV-infected patients, but its etiology is unclear. We describe an HIV-infected patient who presented with fever, wheeze, and micronodular interstitial infiltrates and developed severe hypercapnic and hypoxemic respiratory failure. Open lung biopsy showed necrotizing bronchiolitis with cytopathic changes characteristic of CMV infection; no other pathogens were isolated. He responded well to treatment with ganciclovir.

It has been suggested that thoracic gas volume (TGV) measured in infants in a plethysmograph most accurately represents true lung volume when calculated from end-inspiratory airway occlusions. The rationale proposed is that pressure measured at the mouth underestimates alveolar pressure more at end-expiration than at end-inspiration, presumably due to small airway closure, and this results in greater overestimation of TGV. To investigate this possibility we calculated TGV in 40 wheezy infants from occlusions at both end-inspiration (TGVei) and end-expiration (TGVee) using a 60 L whole body plethysmograph. TGV was corrected for equipment dead space and tidal volume. When a significant change in TGV was defined as lying outside the 95% confidence interval of the TGVee measurements, 8 of the 40 infants tested had significantly higher TGV values measured from occlusions made at end-expiration, while two infants had significantly lower TGV values measured from occlusions made at end-expiration. This trend was not more common in infants with "concave" flow-volume curves. Although it is technically easier to make occlusions at end-expiration, occluding at end-inspiration may minimize errors of TGV measures in a few individuals due to small airway closure at low lung volumes.

Partial expiratory flow-volume curves are commonly used in infant pulmonary function testing. The flow measurements are volume dependent and thoracic gas volume (TGV) is often measured in conjunction with forced expiratory maneuvers. Since it is not possible to make continuous, simultaneous measurements of TGV during forced expiration, it is assumed that lung volume returns to its original value after forced expiration. To test this assumption we measured TGV using a whole body plethysmograph in 14 wheezy infants before and after a series of forced expirations produced with an inflatable jacket. Forced expiration did not cause a significant change in group mean TGV measurements. Examination of individual data did not show any systematic difference between TGV measured before and after forced expiration. These results suggest that repeated forced expirations do not alter TGV within the time scale of usual pulmonary function testing protocols.

Histamine hyperresponsiveness with viral bronchiolitis may depend on previous exposures to viruses or to other pathogens. We studied 32 outbred beagle puppies 80 to 155 days of age who were raised in isolation and who were specific pathogen-free. Puppies were inoculated with canine parainfluenza type 2 (CPI2, n = 8), Bordetella bronchiseptica (Bb, n = 7), or both CPI2 and Bb (CPI2-Bb, n = 9). Control puppies (C, n = 8) were not inoculated. The puppies were anesthetized with sodium thiopental (5 mg/kg) and chloralose (80 mg/kg) and were ventilated mechanically. Lung resistance (RL), dynamic lung compliance (Cdyn), functional residual capacity (FRC), and responsiveness to aerosolized histamine were measured 3 days prior to inoculation (Day -3), on the day of inoculation (Day 0), and on Days 3-4, 6, 8-10, and 12-14 after inoculation. Histamine responsiveness was measured as: (1) the concentration of histamine base that increased RL to 150% (PC 150% RL) or decreased Cdyn to 75% (PC 75% Cdyn) of the response to saline (RL sal and Cdyn sal, respectively), and (2) the change in RL or Cdyn after inhalation of 11 mg/ml of histamine when compared with RL sal and Cdyn sal. On Day 0 there were no significant (p greater than 0.05) differences among groups with regard to age-corrected weights, FRC, RL, Cdyn, or histamine responsiveness. Control puppies remained healthy, and their pulmonary function and histamine responsiveness did not change. CPI2-Bb puppies increased RL and decreased FRC on Day 3-4, and were moderately ill and histamine-hyperresponsive on Day 3-4 and on Day 6.(ABSTRACT TRUNCATED AT 250 WORDS)

About 1% of infants are admitted to hospital with acute bronchiolitis; 85% of cases are caused by infection with Respiratory Syncytial Virus (RSV). The pathophysiological changes during the acute illness are inflammatory obstruction in the small airways with submucosal cellular infiltration, epithelial necrosis and mucous plugging; FRC increases and dynamic compliance falls. Failure to respond to bronchodilator drugs suggests that muscle spasm contributes relatively little to the airway narrowing. Affected infants become increasingly dyspnoeic and hypoxic for 3-4 days then spontaneously improve. After an attack of acute bronchiolitis up to 75% of children have recurrent lower respiratory tract symptoms, many continue to have hyperinflated lungs and bronchial hyperresponsiveness. In the majority, symptoms of cough and wheezing have subsided by the time they start school, but abnormalities of small airway function are detectable at least 13 years later. Children with a genetic predisposition to atopy do not appear to have an increased risk of developing bronchiolitis. Evidence of genetic predisposition to bronchial hyperresponsiveness in those with persistent wheezing is controversial. There is little to suggest that neonatal lung damage or an adverse home environment are important factors in determining susceptibility to post-bronchiolitis wheezing. IgE antibodies to RSV, and leukotriene C4, are found more frequently in the respiratory secretions of infants who wheeze during and after bronchiolitis than in those who do not. The possibility of viral-induced alteration of the immune response at the time of infection needs further investigation.

Measurements of thoracic gas volume, airways resistance, and total respiratory resistance were measured in a group of babies with acute severe bronchiolitis. Assessments were made at convalescence, three to four months later, and after 12 months. Clinical histories were also taken 12 months after the acute episode. Results at this time showed that 35% of the infants had coughing attacks, 50% episodes of wheezing, 50% had dry skin or eczema, and that over 75% had lung function abnormality.

Among 873 children hospitalized with confirmed respiratory viral infections, 492 suffered from bronchopulmonary obstruction. Respiratory syncytial virus infections were dominant among the patients with bronchopulmonary obstruction (80%). The majority of patients with rhinovirus infections suffered from bronchopulmonary obstruction (57%). Two main groups of children at risk from developing bronchopulmonary obstruction during respiratory virus infections were found: 1) infants, suffering from bronchiolitis, mainly due to respiratory syncytial virus, and 2) children of all ages with bronchial asthma, among whom acute attacks were precipitated by virus infections, mainly rhinovirus and respiratory syncytial virus infections. The pathogenesis of bronchopulmonary obstruction during respiratory virus infections is discussed.

High frequency of bronchilitis, 70% of 1117 infants with respiratory infections, and clinical, radiological and laboratory features concerning partial tension of haematic gases, haematic lactate, enzymic activities of serum (CK, GPT, GOT) in 31 infants hospitalized with symptoms of shock in course of respiratory infections apparently affecting the upper respiratory tracts, are reported. This minimal respiratory pathology, evidenced in 3% of 1117 infants, defined as "minimal" viral pneumopathy, can be brought out trough a shock: lactacidosis, combined in half the cases with an increase of serum levels of CK and GPT and with normal PaO2 was ascertained in 87% of the cases. Three groups of bronchiolitis can be differentiated by haemogasanalytic monitoring: 1st group with a "serious" respiratory functional damage (hipercapnia hypoxemia), 14%. 2nd group with a "moderate" damage (normocapnia-hypoxemia), 20%. 3rd group with a "sligth" damage (hypocapnia-normoxemia), 66%. Decompensated shock is considered as a frequent occurrence and it is referred to the widespread involvement of the pulmonary circulation caused by the immunity-flogistic process.

Allergic predisposition among infants with bronchiolitis was examined. The number of infants with serum IgE exceeding mean +1 SD was 31/70 (44.3%). The rate of positive radioallergosorbent test (RAST) scores of 1 or more to mites, egg white, or milk was 31/71 (43.7%) and that of scores over 2 was 11/71 (15.5%). Eosinophils and/or mast cells were found in their nasal smears on several occasions. These results indicated that allergic predisposition may be observed among infants with bronchiolitis.

Cephalexin has had 12 years of extensive clinical usage in the management of respiratory tract and other infections. It is reliably absorbed from the gastrointestinal tract and reaches therapeutic levels in serum and tissues. Toxicity and adverse side effects are minimal. The antimicrobial spectrum includes a majority of the pathogens usually associated with community-acquired lower respiratory tract infections with the significant exception of Haemophilus influenzae. Resistance of H. influenzae strains reduces the uses of cephalexin in the paediatric population and may limit its effectiveness in some patients with acute exacerbations of chronic bronchitis. In contrast, it is inordinately effective in managing most adult patients with lower respiratory tract infections, either as a primary agent, as a substitute for penicillins or other antimicrobial agents in patients unable to receive these, or for continuation of therapy in individuals who no longer require parenteral compounds. As with other cephalosporins, caution should be exercised to exclude meningitis when treating patients with respiratory tract infections since the majority of these compounds, including cephalexin, produce little or no cerebrospinal fluid levels.

From 1974 until April 1977 232 babies with acut bronchiolitis were hospitalized at the Landeskinder-krankenhaus Linz. They represented 8% of all babies admitted to the ward during this period. 9 (= 3,9%) of these were sucessfully mechanically ventilated because of respiratory failure. A pCO2 level above 60 mm Hg was taken as an sign of respiratory insufficiency. By application of artificial ventilation mortality rate of acut bronchiolitis can further be decreased.

During the last 4 years we have seen 13 children with a severe bronchiolitis. The children have had prolonged respiratory illnesses waxing and waning over many months, often requiring oxygen therapy for long periods. The diagnosis is based on a clinical picture similar to acute bronchiolitis, but persisting for months, frequently associated with failure to thrive, coupled with lung function evidence of hyperinflation and airways obstruction but normal static compliance. Confusion with other chronic lung conditions can be clarified by straightforward observations and investigations. We believe that chronic bronchiolitis is fairly common and often misdiagnosed. The short- and medium-term prognosis appears good although small airways disease may persist into adult life.

Apart from cigarette smoking and air pollution, lower respiratory tract infections of viral origin in early childhood are considered to be one of the risk factors for chronic obstructive lung disease. Acute bronchiolitis accounts for the typical disease of the small airways in the first two years of life. 16 symptom-free former patients have been studied 16 to 22 years after an acute attack of bronchiolitis. A complete lung function test was performed with special regard to the small airways. The volume of Isoflow proved to be the most sensitive test. The changes found are considered to be mild. Follow-up will show whether they correlate with an as yet symptom-free stage of a chronic obstructive lung disease.

Report of an 1 1/2 year old boy with the typical features of Williams-Campbell syndrome: chest deformity (thorax piriformis), pulmonary hyperinflation, ballooning of the segmental and subsegmental bronchi during inspiration and collapse with expiration. Atelectasis of the left upper lobe after bronchiolitis obliterans. The literature reports 23 patients with Williams-Campbell syndrome. There is every reason to believe that the extensive bronchiectasis are not due primarily to developmental deficiency of the bronchial cartilage, as the most authors assume, but result from destructive changes after inflammation. In our case very likely an adenovirus infection was the cause. The clinical features of the syndrome look like a severe therapy resistant asthma bronchiale.

Pneumothorax is an uncommon complication of bronchiolitis. The case illustrates an unusual pattern of atelectasis of the right lung with pleural air surrounding the right upper lobe and the remainder of the lung expanded. It is thought that the hyperinflated lung is unable to collapse as a result of the 'ball valve' effect of air trapping.

The clinical and respiratory function characteristics of 200 children 7 years after their admission to hospital with acute lower respiratory tract infection in infancy have been presented. Results were subsequently analysed according to disease category (bronchitis, bronchiolitis, or pneumonia) at initial presentation. Within each diagnostic category recurrent cough and wheeze, a tendency for colds 'to go to the chest', medication, absence from school, and family doctor consultations were significantly increased. Ventilatory function was diminished and bronchial reactivity increased when compared with matched controls. Studies of a different design are required to elucidate the mechanisms whereby symptoms are increased, ventilatory function impaired, and bronchial reactivity increased after severe lower respiratory infection in infancy.

212 Sucklings affected with bronchiolitis were evaluated monitoring values of haematic gases and acid-base balance. The patients were differentiated in three groups: Hypoxemia--Hypercapnia (3.7%). Hypoxemia--Normocapnia (38.2%). Normoxemia--Hypocapnia (58.1%). Metabolic acidosis was detected in 55.1% of cases. The different value of haematic gases was correlated with entity of the pulmonary functional damage.

An unusually large number of infants (82) were admitted to Stanford University Hospital from November 1, 1983, through May 31, 1985, with a diagnosis of bronchiolitis requiring oxygen therapy. A larger percentage of these infants (17/82 = 21%) than generally expected required mechanical ventilation for respiratory failure. Fourteen infants had respiratory syncytial virus (RSV) infections, and three had parainfluenza virus infections. Ten patients had respiratory difficulties as neonates. The mechanical ventilation of the children requiring respiratory assistance was characterized by high minute ventilation with high tidal volumes (15 to 20 ml/kg) and slow respiratory rates (16 to 22 breaths/min). Peak inspiratory pressure averaged (mean +/- SD) 35 +/- 6 cm H2O in the RSV group and 34 +/- 6 cm H2O in the parainfluenza group. The mean number of days on the ventilator was 9.7 +/- 3.1 for the RSV group and 8.3 +/- 2.9 for the parainfluenza group. All were extubated within 17 days of presentation and discharged within 28 days. The complications encountered included pneumothorax and acute pulmonary hypertension.

We reviewed the clinical progress of 81 children as part of a prospective study three and a half years after admission to hospital with acute viral bronchiolitis in infancy. Fifty six (69%) reported episodes of lower respiratory symptoms continuing over the preceding year, 25 (31%) had symptoms lasting for longer than two weeks on two or more occasions, 14 (17%) had symptoms for more than 100 days, and six (7%) required readmission to hospital with acute respiratory illness. Two years previously, these percentages had been 82%, 36%, 33%, and 13% respectively. Forty six (57%) children were said to be improving or to have become asymptomatic, but eight (10%) were deteriorating. There was no difference in the personal or family history of atopy, nor in the rate of skin test positivity between those with and without continuing symptoms, suggesting that atopy does not play an important role in the persistence of symptoms. Less than half the symptomatic children had received bronchodilator treatment during the preceding 12 months.

By better understanding the intrinsic and extrinsic factors that predispose children to chronic lung disease, strategies to prevent its development can be proposed. This article addresses conditions, such as bronchiolitis, croup, hyaline membrane disease, hydrocarbon ingestion, and near-drowning, that have been found to result in long-term changes in lung physiology. Also considered are the possible relationships of common respiratory infection, asthma, smoking, and air pollution to the development of chronic respiratory infection.

A 9-year-old with immunodeficiency developed a severe, diffuse respiratory illness that necessitated mechanical ventilation. Open lung biopsy revealed Respiratory Syncytial Virus (RSV) as the sole pathogen. RSV detection should be included in the differential diagnosis of diffuse lung disease in an immunocompromised child.

A prospective follow-up of 48 infants hospitalized with respiratory syncytial virus bronchiolitis in the first year of life revealed that 44 of these infants had symptoms suggestive of asthma in the 5 years following their initial illness (cumulative prevalence 92%). Symptoms became less frequent and less troublesome during the follow-up period. Thirty-five of these children visited the laboratory for clinical examination, pulmonary function testing, and histamine challenge. Twenty-five children were believed to have clinical evidence of asthma at the time of the laboratory visit (point prevalence 71%). Five children were unable to perform pulmonary function tests; 25 of the remaining 30 (67%) had a positive histamine challenge test. No relationship could be demonstrated between a clinical diagnosis of asthma, a family history of atopy, and the results of histamine challenge testing. These results question the relationship between the results of bronchial provocation tests and clinical asthma in this age group.

In the course of evaluating an infant with recurrent episodes of bronchiolitis, the esophagus was radiologically examined. A totally unexpected finding was the presence of intramural diverticulosis of the upper part of the esophagus. On reexamination four months later, the diverticula had disappeared.

More than one-third of infants with respiratory syncytial virus (RSV) bronchiolitis subsequently experience recurrent episodes of wheezing. In asthmatic children, viral infections frequently trigger asthmatic attacks. Indeed, viruses induce immunological and respiratory functional disorders. As compared with non-wheezing RSV infected infants, wheezing infants with bronchiolitis or asthma due to RSV have: a) increased T-lymphocyte responsiveness to RSV antigen; b) more persistent IgE bound to nasopharyngeal epithelial cells; c) higher titers of RSV-specific IgE and higher histamine concentrations in nasopharyngeal secretions. In children with an atopic constitution, virus infections may trigger allergic sensitization. Furthermore, some viruses enhance the immunologic and non-immunologic human basophil histamine release. Non-specific bronchial hyperreactivity, which is a fundamental feature of asthma, can also be observed to a variable degree in viral respiratory infections. Pulmonary function testing allows in vivo determination of bronchial sensitivity and bronchial reactivity (respectively threshold dose and dose-response curves). Four factors may be involved in bronchoconstriction: a pre-existing diminution of bronchial diameter (which is lacking in many studies); hyperplasia or hypertrophy of bronchial muscles (which is to be excluded in recent viral infections); a non-specific decrease in the threshold for stimulation of irritant receptors due to airway epithelial injury; a partial beta blockade. Further studies are needed to ascertain whether this bronchial hyperreactivity is congenital or acquired.