Streptococcus Pneumoniae Antigens

The life cycle of Streptococcus pneumoniae and the pathogenesis of pneumococcal disease Fig. 1. Schematic depiction of the spread and progression of Streptococcus pneumonia infection (Loughran AJ, et al. 2019)

Molecular mechanisms of pneumococcal colonization of host surfaces Fig. 2 Molecular mechanisms of pneumococcal colonization of host surfaces (Weiser JN, et al. 2018)

Streptococcus pneumoniae (pneumococcus) is a Gram-positive bacterium that is responsible for the majority of community-acquired pneumonia. It is a commensal organism in the human respiratory tract, meaning that it benefits from the human body, without harming it. However, infection by pneumococcus may be dangerous, causing not only pneumonia, but also bronchitis, otitis media, septicemia, and meningitis. Pneumococcal infection is responsible for 1-2 million infant deaths worldwide, every year. S. pneumoniae is alpha-hemolytic, meaning that it can break down red blood cells through the production of hydrogen peroxide (H2O2). The production of H2O2 by the bacterial infection can also cause damage to DNA, and kill cells within the lungs.
The genome of S. pneumoniae is a closed, circular DNA structure that contains between 2.0 and 2.1 million base pairs depending on the strain. It has a core set of 1553 genes, plus 154 genes in its virulome, which contribute to virulence and 176 genes that maintain a noninvasive phenotype. S. pneumoniae produces a range of virulence factors, including capsular polysaccharides, pneumolysin, pneumococcal surface protein A (PspA), pneumococcal surface protein C (PspC), and pneumococcal surface adhesin A (PsaA). There are currently 94 recognized capsular polysaccharide serotypes. Each serotype is distinguished based on the chemical composition of and antigenic differences in the capsular polysaccharide.

  • Polysaccharide capsule has antiphagocytic activity. The capsule prevents iC3b and the Fc of immunoglobulins on the bacterial cell surface from interacting with their receptors on the surface of phagocytic cells, with the result that the organisms remain extracellular. And it also prevents mechanical removal by mucus, and can restrict autolysis and reduce exposure to antibiotics.
  • Pneumolysin belongs to the family of pore-forming toxins and is expressed during the late log phase of growth. The toxin binds to membrane cholesterol, it then forms large pores by the oligomerization of up to 50 toxin monomers. Pneumolysin also mediates other effects at sublytic concentrations, including activation of the classic complement pathway.
  • Pneumococcal surface proteins include lipoproteins, LPXTG proteins, choline-binding proteins and the non-classical surface proteins. The non-classical surface proteins have been identified that do not contain recognized anchor motifs, this family includes pneumococcal adherence and virulence factor A (PavA), glyceraldehyde-3-phosphate dehydrogenase, enolase, and the pneumococcal histidine triad protein (Pht) family.

There are two types of pneumococcal vaccine available on the global market: a pneumococcal vaccine containing purified capsular polysaccharide from 23 of the most common S. pneumoniae serotypes (PPV23) and a pneumococcal conjugate vaccine (PCV10 and PCV13). It is hoped that widespread use of pneumococcal vaccine will not only reduce invasive pneumococcal disease and the rates of otitis media caused by S. pneumoniae but also decrease the incidence of infection with drug-resistant S. pneumoniae. Creative Diagnostics provides the most prevalent serotypes of S. pneumoniae for multiple applications to support your biological programs. Please feel free to contact us.


  1. Loughran AJ, Orihuela CJ, Tuomanen EI. (2019). Streptococcus pneumoniae: Invasion and Inflammation. Microbiology Spectrum. 7(2).
  2. Weiser JN, Ferreira DM, Paton JC. (2018). Streptococcus pneumoniae: transmission, colonization and invasion. Nature Reviews Microbiology. 16, 355–367.
  3. Appelbaum PC. (2002). Resistance among Streptococcus pneumoniae: Implications for Drug Selection. Clinical Infectious Diseases. 34(12), 1613–1620.
  4. Mitchell AM, Mitchell TJ. (2010). Streptococcus pneumoniae: virulence factors and variation. Clinical Microbiology and Infection. 16(5), 411–418.
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