In order to establish infection, the bacteria need to escape the host immune response, and in streptococci, a varied arsenal of bacterial strategies have been described. The M-protein aids in immune evasion by inhibiting phagocytosis and inactivating the complement system.[1] Furthermore, Streptococcus dysgalactiae possesses Protein G, a virulence factor binding circulating immunoglobulins, and thus interfering with the host antibody response.[49] DrsG, a virulence protein abrogating the effect of antimicrobial peptides secreted by human immune cells, is also harboured by a subset of SDSE-strains.[50][51]

Strain Identification to the Species and Subspecies Levels

linical features of upper respiratory tract infection and pyogenic pharyngitis as well as colony counts were tabulated for each patient according to throat culture results.

All isolates were susceptible to penicillin and levofloxacin, 6 (26.1%) showed resistance or reduced susceptibility to erythromycin [1 mef(A), 3 erm(TR), 1 mef(A)+erm(TR) and 1 erm(TR)+erm(B)] and 7 (30.4%) were resistant or exhibited reduced susceptibility to tetracycline [2 tet(M), 5 tet(M)+tet(O)]. The prevalence in Argentina was of at least 23 invasive infections by SDSE. A wide genetic diversity was observed. All isolates carried speJ and ssa genes. Similarly to other studies, macrolide resistance (26.1%) was mainly associated to the MLSB phenotype.