[citation needed] Streptococcus pneumoniae resides asymptomatically in healthy carriers typically colonizing the respiratory tract, sinuses, and nasal cavity.

However, in susceptible individuals with weaker immune systems, such as the elderly and young children, the bacterium may become pathogenic and spread to other locations to cause disease.

These invasive pneumococcal diseases include bronchitis, rhinitis, acute sinusitis, otitis media, conjunctivitis, meningitis, sepsis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.

[7] It consists of a viscous substance derived from a high-molecular-weight polymer composed of repeating oligosaccharide units linked by covalent bonds to the cell wall.

Variations among different S. pneumoniae strains significantly influence pathogenesis, determining bacterial survival and likelihood of causing invasive disease.

[9] In 1881, the organism, known later in 1886 as the pneumococcus[10] for its role as a cause of pneumonia, was first isolated simultaneously and independently by the U.S. Army physician George Sternberg[11] and the French chemist Louis Pasteur.

[15] In 1944, Oswald Avery, Colin MacLeod, and Maclyn McCarty demonstrated that the transforming factor in Griffith's experiment was not protein, as was widely believed at the time, but DNA.

[20] Competence in S. pneumoniae is induced by DNA-damaging agents such as mitomycin C, fluoroquinolone antibiotics (norfloxacin, levofloxacin and moxifloxacin), and topoisomerase inhibitors.

The ability of S. pneumoniae to repair oxidative DNA damage in its genome caused by this host defense likely contributes to the pathogen's virulence.

Consistent with this premise, Li et al.[24] reported that, among different highly transformable S. pneumoniae isolates, nasal colonization fitness and virulence (lung infectivity) depend on an intact competence system.

The transparent phenotype has a thinner capsule and expresses large amounts of phosphorylcholine (ChoP) and choline-binding protein A (CbpA), contributing to the bacteria's ability to adhere and colonize in the nasopharynx.

Here, the infection will spread and cause inflammation, leading to severe disabilities like brain damage or hearing loss or limb removal or death.

[30] Symptoms include common problems such as head aches, fevers, and nausea, but the more telling signs that a bacterial infection may have reached the brain are sensitivity to light, seizures, having limited range in neck movement, and easy bruising all over the body.

The symptoms include confusion, shortness of breath, elevated heart rate, pain or discomfort, over-perspiration, fever, shivering, or feeling cold.

PPV23 functions by utilizing CPS to stimulate the production of type-specific antibodies, initiating processes such as complement activation, opsonization, and phagocytosis to combat bacterial infections.

[48] The recent advances in next-generation sequencing and comparative genomics have enabled the development of robust and reliable molecular methods for the detection and identification of S. pneumoniae.

[49] Atromentin and leucomelone possess antibacterial activity, inhibiting the enzyme enoyl-acyl carrier protein reductase, (essential for the biosynthesis of fatty acids) in S.