Article Text
Abstract
Background Early recognition of children at risk of severe respiratory syncytial virus (RSV) lower respiratory tract infection is important as it informs management decisions. We aimed to evaluate factors associated with severe disease among young children hospitalised with RSV infection.
Methods We conducted a retrospective cohort study of all children <2 years of age hospitalised for RSV lower respiratory tract infection at a single tertiary paediatric hospital over three RSV seasons (January 2017–December 2019). We classified children as having ‘moderate’ or ‘severe’ disease based on the level of respiratory intervention and used univariable and multivariable regression models to determine factors associated with severe disease.
Results Of 970 hospitalised children, 386 (40%) were classified as having ‘severe’ and 584 (60%) as having ‘moderate’ RSV disease. On multivariable analyses, age <2 months (OR: 2.3, 95% CI 1.6 to 3.3, p<0.0001), prematurity (OR: 1.6, 95% CI 1.1 to 2.4, p=0.02) and RSV–parainfluenza virus type 3 (PIV3) codetection (OR: 2.6, 95% CI 1.05 to 6.5, p=0.04) were independently associated with severe disease.
Conclusion Younger age, prematurity and PIV3 codetection were associated with severe RSV disease in children <2 years of age hospitalised with RSV infection. The association between PIV3 and severe RSV disease is a novel finding and warrants further investigation.
- child health
- infectious disease medicine
- paediatrics
- virology
Data availability statement
Data are available in a public, open access repository. Data are available on reasonable request. All data relevant to the study are included in the article or uploaded as supplementary information.
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Data availability statement
Data are available in a public, open access repository. Data are available on reasonable request. All data relevant to the study are included in the article or uploaded as supplementary information.
Footnotes
Contributors JA wrote the manuscript, performed the analyses and aided in the conception of the study. DW conceived the study and study protocol, and provided major input into manuscript revision, analysis and drafting. LAHD performed genotyping experiments and reviewed the laboratory data. MO collected patient data used for the analyses and critically revised the manuscript. LAHD, PVL, KM, KC, GW, A-MC, AD, FEB, NWC and TD contributed to interpretation of the data and critically revised the manuscript. CN contributed to data analysis and interpretation and critically revised the manuscript. LAHD and DW are equally contributed as last authors.
Funding This work was funded by the Murdoch Children’s Research Institute Theme Research Grant. JA is supported by an Australian Postgraduate Award Scholarship. PVL is a recipient of an Australian National Health and Medical Research Council Career Development Fellowship (GNT1146198). We also thank Victorian Government’s Operational Infrastructure Support Program. FEB is a recipient of a National Health and Medical Research Council Practitioner Fellowship and a grant from The Royal Children’s Hospital Foundation.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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