[1] While it has been commonly known that the influenza virus increases one's chances of contracting pneumonia or meningitis caused by the streptococcus pneumonaie bacteria, new medical research in mice indicates that the flu is actually a necessary component for the transmission of the disease.

Inflammation induced by Influenza A Virus (IAV) stimulates the flow of mucus through the expression of glycoproteins, prompts secretion, and increases shedding.

[5]  Streptococcus is found in the inflammation-generated mucus layers covering the URT and increased pneumococci are observed in nasal secretions with IAV co-infection.

Pro-inflammatory effects are exhibited by the single pneumococcal toxin, pneumolysin (Ply); use of anti-Ply antibodies result in decreased inflammation.

[9] Studies have found transmissible levels of bacterium only in young mice, exhibiting that shedding increases with incidences of contact and proximity[failed verification (See discussion.)].

[11] Reduced transmission has been observed amongst children with Pneumococcal conjugate vaccine (PCV) immunization as acquisition of a new strain of S. pneumoniae is inhibited by pre-existing colonization.

Successful colonization requires S. pnuemoniae to evade detection by the nasal mucus and attach to epithelial surface receptors.

[13] However, co-infection with a pre-existing inflammatory URT infection results in an over-expression of the epithelial receptors utilized by S. pneumoniae, thus increasing the likelihood of colonization.

[13] Initial colonization of the nasopharynx is typically asymptomatic, but invasion occurs when the bacteria spreads to other parts of the body including the lungs, blood, and brain.

Interactions between Phosphorylcholine (ChoP) components on colonized epithelial cells allow for docking of choline binding proteins (CBPs), most notably CbpA.

[14] The pneumococcus then moves to invade the lower respiratory tract, evading the mucociliary escalator with the assistance of neuraminidase.