Streptococcus pneumoniae (the pneumococcus) is a commensal of the human nasopharynx during childhood, but also causes a variety of infections, such as otitis media (OM), pneumonia, bacteremia, and meningitis, mainly affecting infants, the elderly, and immunocompromised patients. Pneumococcal pneumonia alone produces more child deaths, every year, than any other bacterial disease worldwide.
To date, more than 100 distinct capsular serotypes have been identified but current pneumococcal conjugate vaccines (PCV10, PCV13, PCV20), and pneumococcal polysaccharide vaccine (PPSV23) protect against up to 23 different pneumococcal types. These vaccines have decreased the burden of pneumococcal disease produced by vaccine types (VT) but provide poor protection against non-vaccine serotypes (NVT) and non-encapsulated S. pneumoniae (NES) strains. Additionally, the increasing prevalence of NVTs, NES and multi-drug resistant S. pneumoniae strains results in more challenge for the treatment of pneumococcal infections. Therefore, it is imperative to continue investigating the transmission, colonization, and molecular pathogenesis of the pneumococcus but also to contribute to our understanding of events leading to an increased resistance to antibiotics.
There are currently a variety of fitness and virulence determinants known to be involved in key aspects of the pathogenesis of pneumococcal disease; some of them are already being tested as a protein-based vaccine. Virulence factors and host immune defense are major players during pathogen-host interactions. Metabolic pathways have also been shown to play a role in pneumococcal pathogenesis. These metabolic pathways include proteins involved in copper efflux, arginine metabolism, and zinc homeostasis. From the human host side, new host factors have been found to play essential roles in the clearance of S. pneumoniae during infection. Moreover, biofilm-like structures may alter both pneumococcal phenotypes and the host immunity during nasopharyngeal carriage and/or during disease. Understanding the overall interaction between pneumococcus and its human host, leading to transmission, colonization and disease, is key for our future fight against pneumococcal infections.
It has been well known for several years that pneumococcal pneumonia is worsened during poly-microbial infection and co-infection. During the past few years, particularly during the CODIV-19 pandemic, rapid progress has been made in this area but there is still much to learn about it. For example, colonization with Influenza A virus increases pneumococcal nasal colonization and it is a risk factor for pneumococcal pneumonia. As a result, pneumococcus is the major pathogen associated with mortality in both the 1918 Spanish influenza pandemic and the 2009 H1N1 pandemic. Secondary pneumococcal pneumonia during COViD-19 episodes appears to be common but more work on this subject is warranted. Other important respiratory viruses and bacterial pathogens, such as Moraxella catarrhalis and Haemophilus influenzae, appear to increase the risk of pneumococcal colonization and disease. A better understanding of the molecular mechanism leading to these pathogenic synergisms will provide a fundamental basis for prevention of pneumococcal transmission and/or colonization and the treatment of secondary pneumococcal infection.
The elderly population is more susceptible to pneumococcal infections. Immunosenescence, the overall decline in immunity that occurs with age as well as inflammaging i.e., low-grade chronic inflammation that accompanies aging both contribute to the increased susceptibility of the elderly to pneumococcal infection. In addition to the dysregulated immunity, alteration of the microbiome seen in the elderly may play a role for the susceptibility of infection. Research with elderly populations or using aged animal infection models is shaping our knowledge about pneumococcal disease in different hosts. Advances in this particular area of study can help inform specialized treatment options and significantly reduce the morbidity and mortality caused by pneumococcal infections during this vulnerable period of life.
Overall, this second edition of the Research Topic is aiming to highlight recent advances in our knowledge of transmission, colonization and molecular pathogenesis of pneumococcal diseases. Contributors are encouraged but may not be limited to provide Original Research papers or Reviews on the following topics:
1) recent advances of transmission of pneumococcus in the human population;
2) pneumococcus-host cell interactions;
3) characterization of novel pneumococcal virulence factors and regulation of virulence genes;
4) molecular studies of pneumococcal biofilm biology during colonization, persistence and infection;
5) recent advances on genomics, proteomics, and metabolomics on pneumococcal pathogenesis;
6) mechanism(s) of pneumococcal infection in the elderly and during co- or poly-microbial infection;
7) molecular studies leading to acquisition of antibiotic resistance mechanisms;
8) synergistic interactions between pneumococcus and other pathogens, including SARS-CoV-2, leading to an enhanced transmission, colonization and/or virulence.
Streptococcus pneumoniae (the pneumococcus) is a commensal of the human nasopharynx during childhood, but also causes a variety of infections, such as otitis media (OM), pneumonia, bacteremia, and meningitis, mainly affecting infants, the elderly, and immunocompromised patients. Pneumococcal pneumonia alone produces more child deaths, every year, than any other bacterial disease worldwide.
To date, more than 100 distinct capsular serotypes have been identified but current pneumococcal conjugate vaccines (PCV10, PCV13, PCV20), and pneumococcal polysaccharide vaccine (PPSV23) protect against up to 23 different pneumococcal types. These vaccines have decreased the burden of pneumococcal disease produced by vaccine types (VT) but provide poor protection against non-vaccine serotypes (NVT) and non-encapsulated S. pneumoniae (NES) strains. Additionally, the increasing prevalence of NVTs, NES and multi-drug resistant S. pneumoniae strains results in more challenge for the treatment of pneumococcal infections. Therefore, it is imperative to continue investigating the transmission, colonization, and molecular pathogenesis of the pneumococcus but also to contribute to our understanding of events leading to an increased resistance to antibiotics.
There are currently a variety of fitness and virulence determinants known to be involved in key aspects of the pathogenesis of pneumococcal disease; some of them are already being tested as a protein-based vaccine. Virulence factors and host immune defense are major players during pathogen-host interactions. Metabolic pathways have also been shown to play a role in pneumococcal pathogenesis. These metabolic pathways include proteins involved in copper efflux, arginine metabolism, and zinc homeostasis. From the human host side, new host factors have been found to play essential roles in the clearance of S. pneumoniae during infection. Moreover, biofilm-like structures may alter both pneumococcal phenotypes and the host immunity during nasopharyngeal carriage and/or during disease. Understanding the overall interaction between pneumococcus and its human host, leading to transmission, colonization and disease, is key for our future fight against pneumococcal infections.
It has been well known for several years that pneumococcal pneumonia is worsened during poly-microbial infection and co-infection. During the past few years, particularly during the CODIV-19 pandemic, rapid progress has been made in this area but there is still much to learn about it. For example, colonization with Influenza A virus increases pneumococcal nasal colonization and it is a risk factor for pneumococcal pneumonia. As a result, pneumococcus is the major pathogen associated with mortality in both the 1918 Spanish influenza pandemic and the 2009 H1N1 pandemic. Secondary pneumococcal pneumonia during COViD-19 episodes appears to be common but more work on this subject is warranted. Other important respiratory viruses and bacterial pathogens, such as Moraxella catarrhalis and Haemophilus influenzae, appear to increase the risk of pneumococcal colonization and disease. A better understanding of the molecular mechanism leading to these pathogenic synergisms will provide a fundamental basis for prevention of pneumococcal transmission and/or colonization and the treatment of secondary pneumococcal infection.
The elderly population is more susceptible to pneumococcal infections. Immunosenescence, the overall decline in immunity that occurs with age as well as inflammaging i.e., low-grade chronic inflammation that accompanies aging both contribute to the increased susceptibility of the elderly to pneumococcal infection. In addition to the dysregulated immunity, alteration of the microbiome seen in the elderly may play a role for the susceptibility of infection. Research with elderly populations or using aged animal infection models is shaping our knowledge about pneumococcal disease in different hosts. Advances in this particular area of study can help inform specialized treatment options and significantly reduce the morbidity and mortality caused by pneumococcal infections during this vulnerable period of life.
Overall, this second edition of the Research Topic is aiming to highlight recent advances in our knowledge of transmission, colonization and molecular pathogenesis of pneumococcal diseases. Contributors are encouraged but may not be limited to provide Original Research papers or Reviews on the following topics:
1) recent advances of transmission of pneumococcus in the human population;
2) pneumococcus-host cell interactions;
3) characterization of novel pneumococcal virulence factors and regulation of virulence genes;
4) molecular studies of pneumococcal biofilm biology during colonization, persistence and infection;
5) recent advances on genomics, proteomics, and metabolomics on pneumococcal pathogenesis;
6) mechanism(s) of pneumococcal infection in the elderly and during co- or poly-microbial infection;
7) molecular studies leading to acquisition of antibiotic resistance mechanisms;
8) synergistic interactions between pneumococcus and other pathogens, including SARS-CoV-2, leading to an enhanced transmission, colonization and/or virulence.