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Chronic colonisation of the lungs with Pseudomonas aeruginosa in patients with cystic fibrosis (CF) is associated with reduced lung function and life expectancy. Prevention of chronic colonisation might be achieved by avoidance of, or early and aggressive treatment of, primary P aeruginosa acquisition.1 Segregation of uninfected indivduals from chronically P aeruginosa colonised CF patients is advocated to prevent cross infection.2 As surveillance studies suggest that the airways of healthy children are rarely colonised with P aeruginosa,3 healthy individuals are not regarded as a potential source of P aeruginosa acquisition. In addition, it has been shown that acquisition of P aeruginosa in CF patients is often preceded by a viral respiratory infection.4 We hypothesised that the incidence of P aeruginosa acquisition during periods of acute respiratory infections (ARI) is equal in both healthy and CF individuals, and considerably exceeds the prevalence in asymptomatic children shown in surveillance studies.
We performed systematic oropharyngeal cultures during periods of ARI between November and May in 20 young children with CF of mean (SD) age 3.6 (2.0) years (range 0.1–7.4) and 19 unrelated age matched healthy controls of mean (SD) age 3.6 (1.7) years. All children were negative for P aeruginosa at the start of the study. Subjects were contacted twice a week with a standard questionnaire regarding symptoms of ARI. If any symptom was present a physician performed an oropharyngeal culture. Cultures from CF patients were also taken at routine visits. The study was approved by the local ethics review committee and all parents of the children gave written informed consent.
A mean (SD) number of 7.5 (2.7) (range 2–13) and 5.1 (1.8) (range 2–9) oropharyngeal cultures were taken from CF patients and healthy controls, respectively. During the study period six children with CF (30%) had at least one P aeruginosa positive culture compared with seven (37%) healthy controls. Cultures following a positive culture in healthy children were always negative for P aeruginosa, while in four of six (67%) CF children short term follow up cultures remained positive for P aeruginosa and anti-pseudomonal treatment was started.
This study showed that P aeruginosa acquisition frequently occurs in periods of ARI in both children with CF and healthy controls. While healthy individuals easily clear P aeruginosa, most CF patients remain positive and require anti-pseudomonal treatment. In the present study we sampled during periods of ARI, which are highly related to respiratory viruses in otherwise healthy children.5 In line with former data in CF, these results suggest that respiratory viral infections facilitate P aeruginosa acquisition and colonisation.4 The high prevalence of P aeruginosa in the airways of healthy children during ARI is in contrast with earlier findings which suggest that P aeruginosa colonisation rarely occurs in the airways of healthy individuals.3 Our data could suggest that even healthy individuals with ARI are a potential source for P aeruginosa acquisition in CF patients. If confirmed, it could have major consequences for current segregation policies which simply avoid contacts between CF patients. It might imply limiting contacts between both CF and non-CF individuals in periods of ARI. Or should we conclude that prevention of P aeruginosa acquisition is practically unrealistic?
Our data urge for studies on the relationship between respiratory viral infections and bacteria in CF, and on the transmission of P aeruginosa between healthy individuals and CF patients. New insights might change current prevention rules and might open new approaches to effective prevention of P aeruginosa acquisition in patients with CF. Prophylactic treatment with anti-pseudomonal antibiotics in periods of ARI might be an interesting option.
This work was supported by the Wilhelmina Children’s Hospital Research Fund (fellowship to B E van Ewijk). The funding source had no role in the design and conduct of the study; in the collection, management, analysis, and interpretation of the data; or in the preparation, review or approval of the manuscript.
TW has served as consultant for Pfizer and Abbott; JK has participated in unrestricted educational activities supported by Abbott for which speakers fees were received from 2002 to 2005 and was co-investigator on a clinical trial endorsed by Abbott which was concluded in 2005; CvdE received research grants and speakers fees from GlaxoSmithKline. None of the other authors has any conflict of interest or financial relationships with a commercial entity that has an interest in the subject of this manuscript.
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