Streptococcuspneumoniae is a gram positive bacteria that is alpha haemolytic under aerobicconditions and beta haemolytic under anaerobic conditions. the common host isthe human body is the nasopharynx/ upper respiratory tract.
From here itspreads to the lungs, blood and through the blood brain barrier to themeninges. Streptococcus Pneumoniae is a major cause of both illness and death.The bacterium is the cause of a wide range of diseases including pneumonia,meningitis, sinusitis, otitis media and septicemia. Pneumococci colonise theupper respiratory tract and act as a reservoir for lower respiratory tractinfection and bacteraemia. An estimated 40% or more children, have their upperrespiratory tracts colonised by pneumococci. Healthy people canasymptomatically carry the pneumococci in their upper respiratory tractdepending on their environment and age of onset. The outer surface of the bacteria is enclosed by a polysaccharidecapsule.
Capsular polysaccharides are very diverse and almost 100 capsularserotypes are known. This bacterial capsule is essential in the virulence ofpneumococci as it protects the bacteria from being phagocytosed. Virulence iscaused by the chemical composition of the capsule, reduced expression resultsin the pneumococcal surface being more accessible to antibodies and complement.Capsular polysaccharides easily initiate an immune response, antibodies thattarget the capsules induce opsonophagocytosis to fight infection. Antigenicityof the capsules is specific to the type, even though cross reaction sometimesoccurs due to share polysaccharides. The cell wall of the pneumococcus is madeup of teichoic acid and polysaccharides. It is an anchor for the cell wallassociated proteins, the intense inflammatory reaction that comes withpneumococcal infection is caused by the cell wall. It promotes the entry ofinflammatory cells and initiates the complement cascade and cytokineproduction.
S. Pneumoniae has to adhere to the epithelial lining in order to colonisethe respiratory tract. In the case of asymptomatic colonisation, thepneumococci bind to the cell surface N-acetyl-glucosamine of resting epithelialcells that are not inflamed. Cell-wall associated surface proteins like thepneumococcal surface adhesion A facilitate the adherence to the sugars.
Thesurface proteins also play a role in the hydrophobic and electrostatic characteristicsof pneumococci. Disease doesn’t typically result from colonisation. To go fromasymptomatic colonisation to disease, the host should generate inflammatoryfactors.
Inflammatory factors such as tumour necrosis factor an interleukin 1as seen in the presence of the influenza viral infection are recruited. Theflow of these inflammatory factors alter the numbers and types of receptors onthe target endothelial and epithelial cells. Choline on the cell wall of thepneumococci has increased affinity for one the receptors that gets upregulated,which is the platelet-activating factor receptor.
When S. Pneumoniae binds tothis receptor internalisation is induced and in turn transcellular migration isalso induced. The pneumococci move through the respiratory epithelium andvascular endothelium, hence invading the rest of the host.