Streptococcus pyogenes

Streptococcus pyogenes, also known as group A streptococcus (GAS), is most commonly associated with mild, self-resolving infections of the skin and oropharynx. However, dissemination of the bacteria to normally sterile sites within the body can lead to a variety of invasive conditions that are associated with high morbidity and mortality. In addition, the generation of human cross-reactive antibodies in response to lingering GAS infection can result in the development of post-streptococcal autoimmune sequelae that afflict the organs, joints and CNS. GAS pathogenesis is mediated by an extensive repertoire of extracellular virulence factors. Initial colonization of the skin and oropharynx is facilitated by cell-associated adhesins that bind to multiple components of the host extracellular matrix. While a battery of antiphagocytic molecules allow the organism to persist at the initial site of infection, the production of multiple toxigenic and tissue-destructive virulence factors facilitates the transition from a superficial to an invasive disease phenotype. Despite the continuing susceptibility of GAS to β-lactam antibiotics a resurgence of serious streptococcal disease has been observed over the past 30 years. While the cause of this resurgence is incompletely understood it has been tentatively attributed to the reappearance and/or increased circulation of a highly invasive clone of serotype M1T1 GAS. This shift in the epidemiology of GAS infection highlights the need for increased surveillance of GAS in the community, faster, more reliable diagnostic tests for GAS infection in a clinical setting, and more targeted treatments of invasive GAS disease. Above all, the development of a safe, effective GAS vaccine would prove invaluable.