INHIBITION OF C3 DEPOSITION ON STREPTOCOCCUS-EQUI SUBSP EQUI BY M-PROTEIN - A MECHANISM FOR SURVIVAL IN EQUINE BLOOD

The effect of the M protein of Streptococcus equi subsp. equi on complement deposition, complement degradation, and bacterial survival in equine whole blood was examined in vitro. Preincubation of bacteria with rabbit M protein-specific immunoglobulin G (IgG) inhibited the survival of the M(+) strain in whole blood by 20-fold (P < 0.01). In addition, preincubation of bacteria with M protein-specific F(ab')(2) fragments inhibited the survival of M(+) cells in whole blood by 3.8 fold (P < 0.01). In the absence of specific antibody, an M(+) strain (CF32) of S. equi subsp. equi survived 100-fold better in whole blood than an M(-) isolate (strain 19) (P < 0.01). Complement inactivation by cobra venom factor significantly enhanced the ability of the M(-) and MC strains of S. equi subsp. equi to survive in whole blood, the latter in the presence or absence of M protein-specific IgG. The major opsonic forms of C3, C3b and iC3b, were present on both M(-) and M(+) cells after opsonization in nonimmune plasma. However, colloidal gold staining indicated that the M(-) strain bound four times as much C3 as the M(+) strain (P < 0.02) and that preincubation of the M(+) strain with M protein-specific IgG or F(ab')(2) fragments also enhanced the amount of C3 deposited by a factor of 4 (P < 0.02). Therefore, at least part of the M protein's ability to enhance bacterial survival in equine whole blood may be related to its ability to interfere with the deposition of equine complement on the bacterial surface.