Research advancements in the field
While it has been commonly known that the influenza virus increases ones 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. Researcher Dimitri Diavatopoulo from the Radboud University Nijmegen Medical Centre in the Netherlands describes his observations in mice, stating that in these animals, the spread of the bacteria only occurs between animals already infected with the influenza virus, not between those without it. He says that these findings have only been inclusive in mice, however, he believes that the same could be true for humans. Mechanism of disease manifestation
Three stages can be used to categorize the infection process of pneumococcal pneumonia: transmission, colonization, and invasion. The Streptococcus pneumoniae (S. pneumoniae) leave the colonized host via shedding in order to be transmissible to new hosts, and must survive in the environment until infection of a new host (unless direct transmission occurs). Animal models have allowed scientists to have an increased understanding of these stages of infection. Transmission
In order for transmission to occur, there must be close contact with a carrier or amongst carriers. The likelihood of this increases during colder, dryer months of the year. The probability of transmission is shown to proliferate in coordination with other upper respiratory tract (URT) infections. Animal models have allowed for an increased understanding of the transmission stage during infection.
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.