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Journal of Clinical Microbiology, June 2007, p. 1690-1696, Vol. 45, No. 6
0095-1137/07/$08.00+0     doi:10.1128/JCM.01912-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Molecular Investigations of an Outbreak of Parainfluenza Virus Type 3 and Respiratory Syncytial Virus Infections in a Hematology Unit{triangledown}

Hamid Jalal,1,{dagger} David F. Bibby,1 Julie Bennett,1 Rebecca E. Sampson,2,{ddagger} Nicola S. Brink,1 Stephen MacKinnon,2 Richard S. Tedder,1 and Katherine N. Ward1*

Centre for Virology, Department of Infection, Royal Free and University College Medical School (UCL Campus), Windeyer Institute of Medical Sciences, 46 Cleveland Street, London W1T 4JF, United Kingdom,1 Department of Haematology, Royal Free and University College Medical School (Hampstead Campus), Rowland Hill Street, London NW3 2PF, United Kingdom2

Received 14 September 2006/ Returned for modification 19 December 2006/ Accepted 2 March 2007

A large simultaneous outbreak of respiratory syncytial virus (RSV) and parainfluenza type 3 (PIV-3) infections occurred on an adult hematology unit. Implementation of enhanced infection control was complicated by cocirculation of the two different viruses, with prolonged viral shedding from infected patients, and placed great pressure on health care staff; of 27 infected hematopoietic stem cell transplant patients, 9 died, and the unit was closed for 2 months. Retrospective molecular investigation of the virus strains involved in the outbreak was performed by analyzing part of the fusion gene of PIV-3 and part of the glycoprotein gene of RSV. Reverse transcription-PCR on nasopharyngeal aspirates from patients infected before and during the simultaneous outbreak generated amplicons for sequence analysis. A single strain of RSV and a single strain of PIV-3 had spread from person to person within the unit; 7 patients were infected with RSV, 22 were infected with PIV-3, and 4 were infected with both viruses. The PIV-3 outbreak had started at the beginning of August 3 months before the RSV outbreak; it had arisen when PIV-3 was introduced from the community by a patient and passed to another patient, who became chronically infected with the identical strain and, in spite of being nursed in isolation, was most likely the source from which widespread infection occurred in November. Had these early cases been linked to a common PIV-3 strain at the time of diagnosis, enhanced infection control precautions might have prevented the eventual extensive spread of PIV-3, making it much easier to deal with the later RSV outbreak.

* Corresponding author. Mailing address: Centre for Virology (UCL Campus), Department of Infection, Royal Free & University College Medical School, Windeyer Institute of Medical Sciences, 46 Cleveland Street, London W1T 4JF, United Kingdom. Phone: 44 20 7679 9490. Fax: 44 20 7580 5896. E-mail: k.n.ward{at}ucl.ac.uk

{triangledown} Published ahead of print on 28 March 2007.

{dagger} Present address: Clinical Microbiology & Public Health Laboratory, Box 236, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QW, United Kingdom.

{ddagger} Present address: Royal Berkshire Hospital, Reading, Berkshire RG1 5AN, United Kingdom.

Journal of Clinical Microbiology, June 2007, p. 1690-1696, Vol. 45, No. 6
0095-1137/07/$08.00+0     doi:10.1128/JCM.01912-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Piralla, A., Percivalle, E., Di Cesare-Merlone, A., Locatelli, F., Gerna, G. (2009). Multicluster nosocomial outbreak of parainfluenza virus type 3 infection in a pediatric oncohematology unit: a phylogenetic study. haematol 94: 833-839 [Abstract] [Full Text]  


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