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Secondary Bacterial Pneumonia by Staphylococcus aureus Following Influenza A Infection Is SaeR/S Dependent

Timothy R Borgogna1, Bennett Hisey1, Emily Heitmann1

  • 1Department of Microbiology and Immunology, Montana State University, Bozeman.

The Journal of Infectious Diseases
|April 19, 2018
PubMed

Insights

Influenza A virus infection enhances Staphylococcus aureus pneumonia. Bacterial response to the lung environment, regulated by SaeR/S, dictates disease severity and fatal outcomes.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Pathogenesis

Background:

  • Staphylococcus aureus is a leading cause of fatal pneumonia after influenza A virus (IAV) infection.
  • The interaction between IAV and S. aureus exacerbates respiratory infections.

Purpose of the Study:

  • To investigate how prior IAV infection influences S. aureus virulence gene expression.
  • To understand the role of the SaeR/S regulatory system in S. aureus pathogenesis post-IAV infection.

Main Methods:

  • Utilized a murine model to compare S. aureus strains USA300 and USA300ΔsaeR/S.
  • Analyzed bacterial virulence gene expression in response to IAV infection.

Main Results:

  • S. aureus pathogenesis following IAV infection is dependent on the SaeR/S regulatory system.
  • IAV infection alters the lung environment, promoting rapid upregulation of S. aureus virulence factors regulated by SaeR/S.
  • Bacterial sensing and response to the lung environment significantly impact pneumonia severity.

Conclusions:

  • The SaeR/S system is crucial for S. aureus virulence in the context of IAV infection.
  • IAV-induced environmental changes in the lung directly influence S. aureus virulence factor expression.
  • Host outcome in secondary bacterial pneumonia is determined by the pathogen's ability to adapt to the host environment.

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