Related Experiment Video
Updated: Sep 21, 2025

Author Spotlight: Advancements in Multiplex Detection of Respiratory Viruses
Published on: November 10, 2023
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.
Abstract:
Secondary bacterial infections can exacerbate SARS-CoV-2 infection, but their prevalence and impact remain poorly understood. Here, we established that a mild to moderate infection with the SARS-CoV-2 USA-WA1/2020 strain increased the risk of pneumococcal (type 2 strain D39) coinfection in a time-dependent, but sex-independent, manner in the transgenic K18-hACE2 mouse model of COVID-19. Bacterial coinfection increased lethality when the bacteria was initiated at 5 or 7 d post-virus infection (pvi) but not at 3 d pvi. Bacterial outgrowth was accompanied by neutrophilia in the groups coinfected at 7 d pvi and reductions in B cells, T cells, IL-6, IL-15, IL-18, and LIF were present in groups coinfected at 5 d pvi. However, viral burden, lung pathology, cytokines, chemokines, and immune cell activation were largely unchanged after bacterial coinfection. Examining surviving animals more than a week after infection resolution suggested that immune cell activation remained high and was exacerbated in the lungs of coinfected animals compared with SARS-CoV-2 infection alone. These data suggest that SARS-CoV-2 increases susceptibility and pathogenicity to bacterial coinfection, and further studies are needed to understand and combat disease associated with bacterial pneumonia in COVID-19 patients.
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.
More Related Videos
12:21A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness
Published on: September 28, 2022
07:30Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
Published on: June 15, 2019
Related Concept Videos
Factors Affecting the Risk of Infection
The integrity and count of the white blood cells help the body resist pathogens and fight infection. When impaired, it reduces the body's resistance to pathogens. The acidic pH levels of the gastrointestinal, genitourinary tracts, and skin...
Stages of Infection
Pulmonary Tuberculosis I
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
Mode of...
Pneumonia II: Pathophysiology
Pulmonary Tuberculosis II
Here is a detailed explanation of its pathophysiology:
Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
Infection
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...