Pneumonia is among the leading causes of illness and death in children <5 years of age worldwide. There is little information on the viral etiology of severe pneumonia in low-income countries, where the disease burden is particularly high.
We analyzed nasopharyngeal aspirates from 629 children 2 to 35 months of age meeting World Health Organization criteria for severe pneumonia and presenting at Kanti Children's Hospital, Kathmandu, Nepal, from January 2006 through June 2008. We examined one specimen from each child for 7 respiratory viruses using reverse transcription polymerase chain reaction.
We detected one or more respiratory viruses in 188 (30%; confidence interval: 26.4%–33.7%) of the 627 specimens with a valid polymerase chain reaction result, of which 88 (14%) yielded respiratory syncytial virus (RSV), 28 (4.5%) influenza A, 24 (5.8%) parainfluenza virus (PIV) type 3, 23 (3.7%) PIV type 1, 17 (2.7%) influenza B, 9 (1.4%) human metapneumovirus, and 5 (0.8%) PIV type 2. Episodes of severe pneumonia occurred in an epidemic pattern with 2 main annual peaks, the viral infections contributing importantly to these epidemics. The largest peaks of severe pneumonia coincided with peaks of RSV infection, which occurred during the last part of the monsoon season and in winter.
RSV was the dominant respiratory viral pathogen detected in young Nepalese children hospitalized with severe pneumonia.
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From the *Department of Microbiology and Infection Control, University Hospital of North Norway, Tromsø, Norway; †Centre for International Health, University of Bergen, Bergen, Norway; ‡Child Health Department, Institute of Medicine, Tribhuvan University, Kathmandu, Nepal; §Department of Microbiology, Tribhuvan University Teaching Hospital, Kathmandu, Nepal; ¶Division of Epidemiology, Department of Epidemiology, Statens Serum Institut, Copenhagen, Denmark; ‖Division of Infectious Disease Control, Norwegian Institute of Public Health, Oslo, Norway; and **Medical Microbiology, Department of Laboratory Medicine, Innlandet Hospital Trust, Lillehammer, Norway.
Accepted for publication July 6, 2011.
Supported by a grant from the European Commission (EU-INCO-DC contract number INCO-FP6-003740). It also received grants from the Norwegian Research Council (RCN project numbers 151054 and 172226) and the Meltzer Foundation in Bergen. The sponsors of the study had no role in study design, collection, analysis and interpretation of data, or writing of the report.
The authors have no other funding or conflicts of interest to disclose.
The corresponding author had full access to all the data in the study and took the final decision to submit this report for publication.
Address for correspondence: Maria Mathisen, PhD, Department of Microbiology and Infection Control, University Hospital of North Norway, Box 56, N-9038 Tromsø, Norway. E-mail: firstname.lastname@example.org.
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