Time-Dependent Increase in Susceptibility and Severity of Secondary Bacterial Infections During SARS-CoV-2

Amanda P Smith1, Evan P Williams2, Taylor R Plunkett2

  • 1Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN, United States.

Insights

SARS-CoV-2 infection increases the risk of secondary pneumococcal coinfection, leading to higher mortality and altered immune responses. This highlights the need for further research into combating bacterial pneumonia in COVID-19 patients.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Virology

Background:

  • Secondary bacterial infections complicate SARS-CoV-2 (COVID-19) outcomes.
  • The prevalence and impact of these coinfections are not fully understood.

Purpose of the Study:

  • To investigate the impact of SARS-CoV-2 infection on susceptibility to secondary bacterial coinfection.
  • To characterize the immune response and pathogenicity of pneumococcal coinfection in a COVID-19 mouse model.

Main Methods:

  • Utilized a transgenic K18-hACE2 mouse model infected with SARS-CoV-2 USA-WA1/2020.
  • Introduced Streptococcus pneumoniae (strain D39) at different time points post-virus infection (pvi).
  • Assessed lethality, bacterial outgrowth, immune cell populations, and cytokine profiles.

Main Results:

  • SARS-CoV-2 infection increased pneumococcal coinfection risk in a time-dependent manner.
  • Bacterial coinfection at 5 or 7 days pvi, but not 3 days pvi, increased lethality.
  • Coinfection altered immune cell populations (neutrophilia, reduced lymphocytes) and cytokine levels, particularly at later time points.
  • Viral load and lung pathology were largely unaffected by bacterial coinfection.

Conclusions:

  • SARS-CoV-2 infection enhances susceptibility and pathogenicity to secondary bacterial coinfection.
  • Immune responses in surviving coinfected animals showed persistent, exacerbated activation in the lungs.
  • Further research is crucial for managing bacterial pneumonia in COVID-19 patients.

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