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Infection and Immunity, July 2006, p. 4014-4020, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.01237-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Pneumococcal Neuraminidases A and B Both Have Essential Roles during Infection of the Respiratory Tract and Sepsis

Sonia Manco,1 Fidelma Hernon,1 Hasan Yesilkaya,1 James C. Paton,2 Peter W. Andrew,1 and Aras Kadioglu1*

Department of Infection, Immunity and Inflammation, University of Leicester, Leicester LE1 9HN, United Kingdom, and,1 School of Molecular and Biomedical Science, University of Adelaide, Adelaide 5005, Australia2

Received 1 August 2005/ Returned for modification 11 November 2005/ Accepted 8 March 2006

We examined the role of the neuraminidases NanA and NanB in colonization and infection in the upper and lower respiratory tract by Streptococcus pneumoniae, as well as the role of these neuraminidases in the onset and development of septicemia following both intranasal and intravenous infection. We demonstrated for the first time using outbred MF1 mouse models of infection that both NanA and NanB were essential for the successful colonization and infection of the upper and lower respiratory tract, respectively, as well as pneumococcal survival in nonmucosal sites, such as the blood. Our studies have shown that in vivo a neuraminidase A mutant is cleared from the nasopharynx, trachea, and lungs within 12 h postinfection, while a neuraminidase B mutant persists but does not increase in either the nasopharynx, trachea, or lungs. We also demonstrated both neuraminidase mutants were unable to cause sepsis following intranasal infections. When administered intravenously, however, both mutants survived initially but were unable to persist in the blood beyond 48 h postinfection and were progressively cleared. The work presented here demonstrates the importance of pneumococcal neuraminidase A and for the first time neuraminidase B in the development of upper and lower respiratory tract infection and sepsis.

* Corresponding author. Mailing address: Department of Infection, Immunity and Inflammation, University of Leicester, P.O. Box 138, University Rd., Leicester LE1 9HN, United Kingdom. Phone: 44 116 2231556. Fax: 44 116 2525030. E-mail: ak13{at}le.ac.uk.

Editor: F. C. Fang

Infection and Immunity, July 2006, p. 4014-4020, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.01237-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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