From the authors:
We thank M. Korppi and co-workers for their correspondence regarding our article [1]. In our prospective study, we identified rhinovirus (RV) infection and a positive family history for asthma as substantial risk factors for recurrent wheezing during 1-yr follow-up after the initial episode of bronchiolitis. The distinctive point of our study was that all the infants enrolled had clinically well-characterised bronchiolitis, defined as the first episode of acute lower airway infection that appears with a history of upper respiratory tract infection followed by acute onset respiratory distress with cough, tachypnoea, retraction and diffuse crackles on auscultation in infants <12 months of age [2]. Another strength of our study is that we also assayed nasal washes simultaneously for 14 different respiratory viruses, rather than just including infants with respiratory syncytial virus bronchiolitis.
We agree with M. Korppi and co-workers that some controversies remain in defining bronchiolitis. The North American definition of bronchiolitis includes the first episode of acute viral wheeze occurring in infants <2 yrs of age [3], thus probably overlapping early asthma manifestations. Defining bronchiolitis according to strict clinical criteria that exclude wheeze ensured the availability of homogeneous studies suitable for investigating epidemiological, clinical and prognostic factors in infants with bronchiolitis. As Jartti et al. [4] underlined, if poorly defined, the diagnosis of bronchiolitis is likely to include various disease entities differing in immunopathogenesis according to viral aetiology, wheezing phenotype and preceding inflammatory state (atopy or no atopy). Another future research direction could be whether the aetiology differs in infants <12 months of age with lower respiratory infections with and without wheeze.
As M. Korppi and co-workers mention, the virus detection rate in our study was rather low (55.6%). Although possible reasons include difficulties in nasal washing or sample storage, we cannot exclude a pathogenetic role in bronchiolitis of viruses other than the 14 investigated. M. Korppi and co-workers noted that only 39 infants were prospectively enrolled as controls. These were consecutive unselected infants with an acute disease unrelated to the respiratory system, hospitalised in our paediatric department. We agree that the small number of patients could be a limitation, but our study was not designed as a community-based control study. All 39 control families and 83.7% of the 313 families of infants with bronchiolitis contacted replied. The only reason for dropout was a change in telephone number.
Our previous study provides reliable data that infants with RV bronchiolitis seem to be those predisposed to asthma, as suggested by the high blood eosinophil counts and heredity for asthma [2]. The question of whether RV is directly involved in the development of asthma or preferentially infects infants prone to wheeze remains unanswered. RV bronchiolitis might serve to disclose infants who are already predisposed to asthma owing to abnormal lung physiology or cytokine dysregulation, or both. Indeed, RV seems preferentially to affect the lower airways, causing bronchiolitis in atopic children prone to wheezing [5].
The lower blood C-reactive protein concentration and fewer radiologically documented lung consolidations in infants with recurrent wheezing than in nonwheezing infants also suggests that the two groups of infants differ not only in having risk factors for atopy and asthma, but also in their pathogenetic response to the different viruses.
In conclusion, we think the time is right to reach an agreement on how to define bronchiolitis. Only by speaking the same language can we understand the pathophysiology and find the optimal therapy for this disease.
Footnotes
Statement of Interest
None declared.
- ©ERS 2012
