Joanna Merckx1,2, Francine M Ducharme3,4, Christine Martineau5,6, Roger Zemek7,8, Jocelyn Gravel3, Dominic Chalut9, Naveen Poonai10, Caroline Quach11,5,12. 1. Division of Infectious Diseases, Department of Pediatrics. 2. Department of Epidemiology, Biostatistics, and Occupational Health, McGill University, Montreal, Quebec, Canada. 3. Departments of Pediatrics and. 4. Social and Preventive Medicine, CHU Sainte-Justine, University of Montreal, Quebec, Canada. 5. Department of Microbiology, Infectious Disease, and Immunology, University of Montreal, Montreal, Quebec, Canada. 6. Laboratoire de Santé Publique du Québec, Institut National de Santé Publique du Québec, Sainte-Anne-de-Bellevue, Canada. 7. Department of Pediatrics and Emergency Medicine, University of Ottawa, Ottawa, Ontario, Canada. 8. Children's Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada; and. 9. The Montreal Children's Hospital, McGill University, Montreal, Quebec, Canada. 10. Children's Hospital, London Health Sciences Centre, London, Ontario, Canada. 11. Department of Epidemiology, Biostatistics, and Occupational Health, McGill University, Montreal, Quebec, Canada; c.quach@umontreal.ca. 12. Infection Prevention and Control Unit, Division of Infectious Disease and Medical Microbiology, CHU Sainte-Justine, Montreal, Quebec, Canada.
Abstract
: media-1vid110.1542/5771275574001PEDS-VA_2017-4105Video Abstract OBJECTIVES: Respiratory pathogens commonly trigger pediatric asthma exacerbations, but their impact on severity and treatment response remains unclear. METHODS: We performed a secondary analysis of the Determinants of Oral Corticosteroid Responsiveness in Wheezing Asthmatic Youth (DOORWAY) study, a prospective cohort study of children (aged 1-17 years) presenting to the emergency department with moderate or severe exacerbations. Nasopharyngeal specimens were analyzed by RT-PCR for 27 respiratory pathogens. We investigated the association between pathogens and both exacerbation severity (assessed with the Pediatric Respiratory Assessment Measure) and treatment failure (hospital admission, emergency department stay >8 hours, or relapse) of a standardized severity-specific treatment. Logistic multivariate regressions were used to estimate average marginal effects (absolute risks and risk differences [RD]). RESULTS: Of 958 participants, 61.7% were positive for ≥1 pathogen (rhinovirus was the most prevalent [29.4%]) and 16.9% experienced treatment failure. The presence of any pathogen was not associated with higher baseline severity but with a higher risk of treatment failure (20.7% vs 12.5%; RD = 8.2% [95% confidence interval: 3.3% to 13.1%]) compared to the absence of a pathogen. Nonrhinovirus pathogens were associated with an increased absolute risk (RD) of treatment failure by 13.1% (95% confidence interval: 6.4% to 19.8%), specifically, by 8.8% for respiratory syncytial virus, 24.9% for influenza, and 34.1% for parainfluenza. CONCLUSIONS: Although respiratory pathogens were not associated with higher severity on presentation, they were associated with increased treatment failure risk, particularly in the presence of respiratory syncytial virus, influenza, and parainfluenza. This supports influenza prevention in asthmatic children, consideration of pathogen identification on presentation, and exploration of treatment intensification for infected patients at higher risk of treatment failure.
: media-1vid110.1542/5771275574001PEDS-VA_2017-4105Video Abstract OBJECTIVES:Respiratory pathogens commonly trigger pediatric asthma exacerbations, but their impact on severity and treatment response remains unclear. METHODS: We performed a secondary analysis of the Determinants of Oral Corticosteroid Responsiveness in Wheezing Asthmatic Youth (DOORWAY) study, a prospective cohort study of children (aged 1-17 years) presenting to the emergency department with moderate or severe exacerbations. Nasopharyngeal specimens were analyzed by RT-PCR for 27 respiratory pathogens. We investigated the association between pathogens and both exacerbation severity (assessed with the Pediatric Respiratory Assessment Measure) and treatment failure (hospital admission, emergency department stay >8 hours, or relapse) of a standardized severity-specific treatment. Logistic multivariate regressions were used to estimate average marginal effects (absolute risks and risk differences [RD]). RESULTS: Of 958 participants, 61.7% were positive for ≥1 pathogen (rhinovirus was the most prevalent [29.4%]) and 16.9% experienced treatment failure. The presence of any pathogen was not associated with higher baseline severity but with a higher risk of treatment failure (20.7% vs 12.5%; RD = 8.2% [95% confidence interval: 3.3% to 13.1%]) compared to the absence of a pathogen. Nonrhinovirus pathogens were associated with an increased absolute risk (RD) of treatment failure by 13.1% (95% confidence interval: 6.4% to 19.8%), specifically, by 8.8% for respiratory syncytial virus, 24.9% for influenza, and 34.1% for parainfluenza. CONCLUSIONS: Although respiratory pathogens were not associated with higher severity on presentation, they were associated with increased treatment failure risk, particularly in the presence of respiratory syncytial virus, influenza, and parainfluenza. This supports influenza prevention in asthmatic children, consideration of pathogen identification on presentation, and exploration of treatment intensification for infectedpatients at higher risk of treatment failure.
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