The genome of Streptococcus pyogenes is 1.8-Mbp long and codes for about 1700-1900 proteins (Beres SB, 2006).
Besides the factors that code for virulence, S. pyogenes have been observed to have other plasmids. In India, researchers isolated colonies with pA852 and pA996 plasmids. These carried known or potential bacteriocin genes (Bergmann, 2014). In Sweden, researchers have studied erythromycin resistance plasmids in S. pyogenes. These resistance plasmids are pSE701, pSE702, and pSE703 (Schalén C, 2019). S. pyogenes can become competent, so the occurrence of specific plasmids can vary (Suvorov, 2000).
S. pyogenes contains a variety of virulence/toxin factors which can be illustrated with the mnemonic “SMASHED”; Streptolysins, M protein, Anti-C5a peptidase, Streptokinase, Hyaluronidase and Hyaluronic acid capsule, Exotoxin, and DNAses(Terao, 2012).
- Streptolysin O is a 540-amino-acid protein that binds to cholesterol in eukaryotic cell membranes creating pores leading to cell lysis, this is coded by the slo operon(Fontaine, 2003).
- M proteins help the bacteria resist phagocytosis and cover the cell, they are coded by M genes, there’s more than 200 variants coded for by M6 gene, M12 gene, M18 gene and so on(Fischetti, 2016).
- Anti-C5a peptidase is coded by a gene named scpB and functions to help the bacteria bind to it’s hosts cells(Beckmann, 2002).
- Streptokinase is coded by a gene named SK and helps to make the cell more ‘sticky’(Huish, 2017).
- Hyaluronidase is coded by the hylA gene and is responsible for making the organism capable of degrading body tissue(Hynes, 2000).
- Erythrogenic toxin, or exotoxin is coded for in the speA gene(C R Weeks, 1984).
- There are several genes responsible for at least 8 DNAases in S. Pyogenes(Remmington, 2018).
Mutations of S. pyogenes have been isolated from patients that were infected by the wild-type S. pyogenes. In some cases, a mutant has a high frequency of mutations in the sic promoter, this made the organisms express more key virulence genes causing the patient to have toxic-shock syndrome from a typical infection (Ikebe, 2016).
Other mutations occur where the wild-type obtains a plasmid from a bacteriophage. This can increase the expression of genes that code for a variety of exotoxins (C R Weeks, 1984).
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Beckmann, C. (2002). Identification of Novel Adhesins from Group B Streptococci by Use of Phage Display Reveals that C5a Peptidase Mediates Fibronectin Binding. Infection And Immunity.
Beres SB, R. E. (2006). Molecular genetic anatomy of inter- and intraserotype variation in the human bacterial pathogen group a Streptococcus. Proceedings of the National Academy of Sciences, 10-14.
Bergmann, R. N.-S. (2014). Distribution of small native plasmids in Streptococcus pyogenes in India. International Journal Of Medical Microbiology, 304.
C R Weeks, J. (1984). The gene for type A streptococcal exotoxin (erythrogenic toxin) is located in bacteriophage T12. Infection And Immunity.
Fischetti, V. (2016). M Protein and Other Surface Proteins on Streptococci. University Of Oklahoma Health Sciences Cente.
Fontaine, M. L. (2003). Combined Contributions of Streptolysin O and Streptolysin S to Virulence of Serotype M5 Streptococcus pyogenes Strain Manfredo. Infection And Immunity.
Huish, S. T. (2017). Activity Regulation by Fibrinogen and Fibrin of Streptokinase from Streptococcus Pyogenes. PLOS ONE Journal.
Hynes, W. D. (2000). The extracellular hyaluronidase gene (hylA) of Streptococcus pyogenes. FEMS Microbiology Letter, 109-112.
Ikebe, T. M. (2016). Spontaneous mutations in Streptococcus pyogenes isolates from streptococcal toxic shock syndrome patients play roles in virulence. Scientific Reports.
Remmington, A. &. (2018). The DNases of pathogenic Lancefield streptococci. Microbiology.
Schalén C, e. (2019). Characterization of an erythromycin resistance (erm) plasmid in Streptococcus pyogenes. PubMed – NCBI.
Suvorov, A. &. (2000). Replication origin of Streptococcus pyogenes, organization and cloning in heterologous systems. FEMS Microbiology Letters, 293-297.
Terao, Y. (2012). The virulence factors and pathogenic mechanisms of Streptococcus pyogenes. Journal Of Oral Biosciences, 54.