Abstract
Chronic cough in children is common and frequently mismanaged. In the past, cough was diagnosed as asthma and inappropriate asthma therapies prescribed and escalated. It has been realized that persistent bacterial bronchitis (PBB) is a common cause of wet cough and responds to oral antibiotics. The initial definition comprised a history of chronic wet cough, positive bronchoalveolar (BAL) cultures for a respiratory pathogen and response to a 2-week course of oral amoxicillin–clavulanic acid. This is now termed PBB-micro; PBB-clinical eliminates the need for BAL. PBB-extended is PBB-micro or PBB-clinical but resolution necessitating 4 weeks of antibiotics; and recurrent PBB is >3 attacks of PBB-micro or-clinical/year. However, the airway has only a limited range of responses to chronic inflammation and infection, and neutrophilic airway disease is seen in many other conditions, such as cystic fibrosis and primary ciliary dyskinesia, both chronic suppurative lung disease endotypes, whose recognition has led to huge scientific and clinical advances. There is an urgent need to extend endotyping into PBB, especially PBB-recurrent. We need to move from associative studies and, in particular, deploy sophisticated modern –omics technologies and systems biology, rather as has been done in the context of asthma in U-BIOPRED. In summary, the use of the term PBB has done signal service in pointing us away from prescribing asthma therapies to children with infected airways, but we now need to move beyond a simple description to teasing out underlying endotypes.
Highlights
It has been realized that persistent bacterial bronchitis (PBB) is a common cause of wet cough and responds to oral antibiotics
This led to the catastrophic explosion of asthma mis-diagnoses [1,2,3], when normal children coughing with viral colds were diagnosed as asthmatic, and treatment escalated every time they coughed with another cold, despite ample evidence that escalating asthma therapy above low-dose inhaled corticosteroids is subject to the law of very rapidly diminishing returns [4]
Children were treated with inhaled corticosteroids for eosinophilic airway inflammation with no attempt to demonstrate that airway inflammation was present, and with bronchodilators without seeing if there was true reversible airway obstruction due to constriction of airway smooth muscle; too often we have given these treatments and believed the patient’s subjective impressions
Summary
The initial definition was (i) a history of chronic wet cough, (ii) positive bronchoalveolar (BAL) cultures for a respiratory pathogen, and (iii) response to a 2-week course of oral amoxicillin–clavulanic acid [5]. There is no requirement to try to define infection non-bronchoscopically, with either cough swabs or better, induced sputum which is feasible even in very resource poor settings [15] and very young children [15, 16] and gives results comparable to BAL. This is a sad exemplar of the current “don’t measure” culture of pediatric pulmonology, which is a significant omission, as is the absence of any requirement to test if infection has resolved with antibiotics. It is perfectly clear that the infected airway signals a problem in stereotypic fashion—wet cough, respiratory distress, wheeze related to secretion retention—whether the cause be, for example, anatomical airway obstruction, a local or systemic immunodeficiency, or any one of many aspiration syndromes
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