Complement resistance mechanisms of streptococci

Group A streptococcus (GAS, Streptococcus pyogenes), group B streptococcus (GBS, Streptococcus agalactiae) and pneumococcus (Streptococcus pneumoniae) are all human pathogens that cause significant morbidity and mortality worldwide. These related species cause different spectra of infections spanning from trivial upper respiratory tract or skin infections to septic and severe diseases. In order to cause deep infections and survive in the human body the bacteria must evade the immune system. Complement is an important part of innate immunity both as an opsonizing and membrane destructing cascade and as an effector system of antibodies. In this review, we describe the complement resistance mechanisms of the three clinically most important streptococcal species, groups A and B streptococci and pneumococcus. The complement evasion mechanisms of these three species are analogous, yet different from one another. Several strains of all three species express molecules (M-proteins, Bac or beta, PspC) that acquire host fluid-phase complement regulators factor H or C4b binding protein to their surfaces. Groups A and B streptococci also secrete proteins and/or enzymes that inhibit the activation of the complement system or chemotaxis caused by the complement activation products. Even though a lot is known about the immune evasion by streptococci, the high morbidity and mortality associated with infections caused by streptococci and the need for efficient vaccines warrant further studies on the streptococcal molecules mediating complement resistance.