[Mechanism behind streptococcus toxic shock-like syndrome onset--immune evasion and bacterial properties]

Streptococcal toxic shock-like syndrome (STSS) was firstly reported in 1987 in the United States. Japan's first definitive STSS case was reported in 1992, with over 500 cases since confirmed. Mortality is extremely high at 40%. Pathological findings, bacteria aggregation, and a paucity of polymorphonuclear neutrophils (PMN) in the foci of invasive group A streptococcal (GAS) infection suggest that host defense disturbance plays an important role in invasive infection onset. GAS, clinically isolated from severely invasive, but not from non-invasive, infections, could compromise human PMN functions in at least two independent ways-by inducing necrosis to PMN by enhanced production of pore-forming toxin streptolysin O (SLO) and by PMN migration impairment via digesting interleukin-8, a PMN attracting chemokine, through increased serine protease ScpC production. Expression of these genes was upregulated by a loss of repressive function with the csrS gene mutation of the two-component sensor/regulator system.