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Infection and Immunity, June 2007, p. 3102-3111, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01943-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Filamentous Influenza A Virus Infection Predisposes Mice to Fatal Septicemia following Superinfection with Streptococcus pneumoniae Serotype 3{triangledown}

Janice L. Speshock,1 Nicole Doyon-Reale,1 R. Rabah,2 Melody N. Neely,1 and Paul C. Roberts1*

Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, Michigan 48201,1 Department of Pathology, Children's Hospital of Michigan, Detroit, Michigan 482012

Received 11 December 2006/ Returned for modification 21 January 2007/ Accepted 24 March 2007

Previous studies have demonstrated that animals exposed to Streptococcus pneumoniae while recovering from influenza A virus infection exhibit exacerbated disease symptoms. However, many of the current animal models exploring dual viral and bacterial synergistic exacerbations of respiratory disease have utilized mouse-adapted influenza virus and strains of Streptococcus pneumoniae that in themselves are highly lethal to mice. Here we describe a mouse model of bacterial superinfection in which a mild, self-limiting influenza virus infection is followed by mild, self-limiting superinfection with S. pneumoniae serotype 3. S. pneumoniae superinfection results in rapid dissemination of the bacterium from the respiratory tract and systemic spread to all major organs of the mice, resulting in fatal septicemia. This phenomenon in mice was observed in superinfected animals undergoing an active viral infection as well as in mice that had completely cleared the virus 7 to 8 days prior to superinfection. Neutrophils were the predominant cellular inflammatory infiltrate in the lungs of superinfected mice compared to singly infected animals. Among other cytokines and chemokines, the neutrophil activator granulocyte colony-stimulating factor (G-CSF) was found to be significantly overexpressed in the spleens, lungs, and brains of superinfected animals. High G-CSF protein levels were observed in sera and lung lavage fluid from superinfected animals, suggesting that G-CSF is a major contributor to synergistic exacerbation of disease leading to fatal septicemia.

* Corresponding author. Present address: Department of Biomedical Sciences and Pathobiology, Centers for Molecular Medicine and Infectious Diseases, Virginia Tech, 1410 Prices Fork Road (0342), Blacksburg, VA 24061. Phone: (540) 231-7949. Fax: (540) 231-3426. E-mail: pcroberts{at}vt.edu

{triangledown} Published ahead of print on 2 April 2007.

Editor: A. Camilli

Infection and Immunity, June 2007, p. 3102-3111, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01943-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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