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This study examines the diversity of superantigen gene profiles between and within emm-genotypes of 92 clinical group A streptococcal isolates (30 STSS, 24 sepsis, 25 erysipelas, and 12 tonsillitis) collected in Sweden between 1986 and 2001. The emm-genotype and the distribution of smeZ, speG, speJ, speA, speC, speH, speI, speK/L, speL/M, speM, and ssa genes, and the smeZ allelic variant were determined using PCR and DNA sequencing. Forty-five emm1 isolates revealed 10 superantigen gene profiles. One profile dominated and was identified in 22 isolates collected over 14 years. The results indicate that a selective advantage maintained this genotype in circulation. The superantigen content among the emm1 isolates ranged from three to seven, with smeZ-1, speG, and speA present in all but one profile. The 47 isolates of 27 other emm-genotypes exhibited 29 superantigen gene profiles. Thus, the distribution of superantigen genes was highly variable within isolates regardless of emm-genotype. Two novel emm1 subtypes and 14 novel smeZ allelic variants were identified. The 22 smeZ alleles were generally linked to the emm-genotype. The results of the investigation show that superantigen gene profiling is useful for tracking spread of clones in the community.

The nature of the mitogenic activity of pyrogenic streptococcal exotoxin B, also known as streptococcal cysteine protease, has been debated in the literature. Streptococcal exotoxin B has been shown to cleave interleukin-1beta precursor and create biologically active interleukin-1beta, a major cytokine mediating inflammation and shock. This activity could mimic the mitogenicity and cytokine release induced by superantigens in lymphocyte stimulating experiments. In this study, the protease activity of streptococcal exotoxin B was irreversibly inhibited by covalent binding of a tripeptide and the superantigenic properties of streptococcal exotoxin B were found not to be influenced by this inactivation. Native as well as protease-inactivated streptococcal exotoxin B was shown to stimulate T-cell proliferation without a need of metabolically active antigen presenting cells. Furthermore, streptococcal exotoxin B-induced T-cell proliferation was shown to require HLA-DQ since addition of HLA-DQ monoclonal antibodies totally inhibited the mitogenic activity of streptococcal exotoxin B, indicating that streptococcal exotoxin B, as other superantigens, makes direct contact with the T-cell receptor via HLA class II. The aim of this study was to characterize the relationship between the proteolytic and superantigenic properties of streptococcal exotoxin B.

Two divergently transcribed open reading frames: cpsX and cpsY separated by a common regulatory region was identified upstream of the cpsA-D genes involved in polysaccharide capsule biosynthesis in group B streptococci (GBS). We suggest that these genes are involved in the regulation of capsule expression in GBS, since the CpsX protein shares sequence similarities with LytR of Bacillus subtilis, an attenuator of transcription while CpsY has similarity to a wide variety of members of the LysR family of transcriptional regulators. No deletions, insertions, DNA rearrangements, or apparent differences were discovered in the postulated regulatory genes when the gene region was compared in GBS with different capsule phenotypes. Thus, other yet unidentified gene loci may control capsule phase variation in GBS.