Process of infection
To colonise the throat, GAS must attach to the surface cells of the pharynx. This requires specific adhesion molecules on the bacteria that match surface proteins on the pharyngeal epithelial cells. Poor attachment would allow saliva and cell shedding to remove the GAS and prevent colonisation or infection. There is also evidence of competition between GAS and normal flora for attachment sites.
Once attached, GAS begin multiplying and invade the epithelial cells. They are able to evade immune responses in the host by a variety of mechanisms including, as described above, M-protein inhibition of phagocytosis. The bacteria are also coated in a capsule made of hyaluronic acid--a substance that occurs naturally in the host connective tissue thus they are able to disguise themselves from immune surveillance. (8)
Once the GAS has penetrated the epithelial barrier, the actions of bacterial exotoxins damage the host cell and provoke immune responses. Haemolysins destroy host cells and induce antibody production. Streptococcal pyrogenic exotoxins (SPEs) induce fever (and rash in scarlet fever) and strongly activate the immune system. In toxic shock syndrome, it is these exotoxins that are believed to act as "superantigens", triggering widespread abnormal activation of immune and inflammatory responses. (9) Other exotoxins cause the formation of pus, which provides a growth medium for the bacteria, and enzymes that allow further penetration of the GAS through the host connective tissue.