Streptococcus, Group A, Severity Of Infection By

Since the early 1980s, a resurgence of severe, invasive infections by group A streptococci (GAS; Streptococcus pyogenes) has occurred. The reemergence of streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (NF) has been reported in several countries. Both are rapidly progressive invasive diseases that are associated with high mortality rate, ranging from 30 to 80% despite prompt antibiotic therapy and debridement. A particular subclone of the M1 serotype (M1T1) has persisted for more than 20 years as the most prevalent strain isolated from these infections. Release of inflammatory cytokines triggered by streptococcal superantigens has a pivotal role in invasive streptococcal disease. However, individuals infected with the same strain can develop different manifestations. Kotb et al. (2002) reported that the immunogenetics of the host influence the outcome of invasive streptococcal infection. They found that specific human leukocyte antigen (HLA) class II haplotypes conferred strong protection from severe systemic disease, whereas others increased the risk of severe disease. Patients with the DRB1*1501 (142857)/DQB1*0602 (604305) haplotype mounted significantly reduced responses and were less likely to develop severe systemic disease. Kotb et al. (2002) proposed that class II HLA allelic variation contributes to differences in the severity of invasive streptococcal infections through the ability of distinct HLA alleles/haplotypes to regulate cytokine responses triggered by streptococcal superantigens.