Secondary infection with Streptococcus pneumoniae decreases influenza virus replication and is linked to severe

Karina Mueller Brown1, Valerie Le Sage2, Andrea J French2

  • 1Department of Biological Sciences, Carnegie Mellon University, 4400 Fifth Avenue, Pittsburgh, PA 15213, USA.

FEMS Microbes
|April 8, 2022
PubMed

Insights

Secondary Streptococcus pneumoniae (Spn) infection after H1N1 influenza reduces viral load but worsens bacterial pneumonia. This suggests an asymmetrical, not synergistic, relationship between these pathogens in ferrets.

Area of Science:

  • Infectious diseases
  • Virology
  • Bacteriology

Background:

  • Secondary bacterial infections, particularly Streptococcus pneumoniae (Spn), are common in severe influenza, increasing mortality.
  • The 2009 H1N1 pandemic highlighted the danger of Spn coinfection in young adults.

Purpose of the Study:

  • To investigate the interaction between pandemic H1N1 influenza virus (H1N1pdm09) and secondary Spn infection in a ferret model.
  • To determine the impact of Spn coinfection on H1N1pdm09 replication and airborne transmission.

Main Methods:

  • Ferrets were infected with H1N1pdm09 followed by Spn (strains BHN97, D39) or vice versa.
  • Viral titers in nasal washes and bacterial loads were measured.
  • Airborne transmission of H1N1pdm09 was assessed.
  • Clinical symptoms were monitored.

Main Results:

  • Secondary Spn infection significantly decreased H1N1pdm09 viral titers in ferret nasal washes.
  • Ferrets with H1N1pdm09 and secondary Spn infection showed increased bacterial loads and more severe clinical symptoms.
  • Spn precolonization did not affect H1N1pdm09 airborne transmission susceptibility.
  • Animals with severe coinfection exhibited reduced H1N1pdm09 airborne transmission.

Conclusions:

  • The relationship between H1N1pdm09 and Spn is asymmetrical: Spn enhances its own colonization and pathogenesis but reduces influenza viral load.
  • Secondary bacterial infection exacerbates Spn-related illness but dampens influenza virus replication.
  • Severe coinfection may paradoxically reduce influenza virus airborne transmission.

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