Transmission via the secretions of carriers can result from direct interpersonal contact or contact with a contaminated surface. Bacteria on contaminated surfaces can be easily cultured. In conditions with sufficient nutrients, pneumococci can survive for 24 hours and avoid desiccation for multiple days. 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. Immunoglobulin G (IgG) immunization with high antibody concentration can also inhibit acquisition. These antibodies require the agglutinating function of the Fc fragment. For successful acquisition in a new host, pneumococcus must successfully adhere to the mucous membrane of the new host’s nasopharynx. Pneumococcus is able to evade detection by the mucous membrane when there is a higher proportion of negatively charged capsules. This clearance is mediated by Immunoglobulin A1 (IgA1) which is abundant on the URT mucosal surfaces. Colonization
Transparent and opaque colony morphology has been observed for pneumococci. Airway colonization is observed in transparent phenotypes of serotypes, while survival in bloodstreams is observed for opaque phenotypes. Colonizable strains exhibit resistance against neutrophilic immune response. Successful colonization requires S. pnuemoniae to evade detection by the nasal mucus and attach to epithelial surface receptors. Asymptomatic colonization occurs when S. pneumoniae bind to N-acetyl-glucosamine on epithelium without inflammation. 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.
A 2010 study examining co-infection of influenza in co-housed ferret pairs found that the influenza increased both incidence and severity of pneumococcal infection. These findings exhibited pneumococcal strain dependence. A separate 2010 study examining intra-litter transmission, with influenza co-infection in infant mice, found that the influenza co-infection is a facilitator for pneumococcal susceptibility, transmission, and disease via bacterial shedding. A third study of note, from 2016, was able to examine pneumococcal transmission without co-infection of an URT infection. This study utilized intra-litter transmission in infant mice during bacterial mono-infection with pneumococcus. The results of this study indicated higher rates of shedding for infections in younger mice. These studies, along with the animal models that they utilize have enhanced our understanding of the transmission of pneumococcus. Inflammation induced by Influenza A Virus (IAV) stimulates the flow of mucus through the expression of glycoproteins, prompts secretion, and increases shedding. Streptococcus is found in the inflammation-generated mucus layers covering the URT and increased pneumococci are observed in nasal secretions with IAV co-infection. Levels of shedding have correlations with IAV induced URT inflammation. Pro-inflammatory effects are exhibited by the single pneumococcal toxin, pneumolysin (Ply); use of anti-Ply antibodies result in decreased inflammation. Studies have found transmissible levels of bacterium only in young mice, exhibiting that shedding increases with incidences of contact and proximity. Shedding is shown to decrease in the presence of agglutinating antibodies such as IgG and IgA1 unless cleavage occurs via an IgA1-specific pneumococcal protease.