Abstract
BackgroundStreptococcus dysgalactiae subsp. equisimilis (SDSE) causes invasive streptococcal infections, including streptococcal toxic shock syndrome (STSS), as does Lancefield group A Streptococcus pyogenes (GAS). We sequenced the entire genome of SDSE strain GGS_124 isolated from a patient with STSS.ResultsWe found that GGS_124 consisted of a circular genome of 2,106,340 bp. Comparative analyses among bacterial genomes indicated that GGS_124 was most closely related to GAS. GGS_124 and GAS, but not other streptococci, shared a number of virulence factor genes, including genes encoding streptolysin O, NADase, and streptokinase A, distantly related to SIC (DRS), suggesting the importance of these factors in the development of invasive disease. GGS_124 contained 3 prophages, with one containing a virulence factor gene for streptodornase. All 3 prophages were significantly similar to GAS prophages that carry virulence factor genes, indicating that these prophages had transferred these genes between pathogens. SDSE was found to contain a gene encoding a superantigen, streptococcal exotoxin type G, but lacked several genes present in GAS that encode virulence factors, such as other superantigens, cysteine protease speB, and hyaluronan synthase operon hasABC. Similar to GGS_124, the SDSE strains contained larger numbers of clustered, regularly interspaced, short palindromic repeats (CRISPR) spacers than did GAS, suggesting that horizontal gene transfer via streptococcal phages between SDSE and GAS is somewhat restricted, although they share phage species.ConclusionGenome wide comparisons of SDSE with GAS indicate that SDSE is closely and quantitatively related to GAS. SDSE, however, lacks several virulence factors of GAS, including superantigens, SPE-B and the hasABC operon. CRISPR spacers may limit the horizontal transfer of phage encoded GAS virulence genes into SDSE. These findings may provide clues for dissecting the pathological roles of the virulence factors in SDSE and GAS that cause STSS.
Highlights
Streptococcus dysgalactiae subsp. equisimilis (SDSE) causes invasive streptococcal infections, including streptococcal toxic shock syndrome (STSS), as does Lancefield group A Streptococcus pyogenes (GAS)
These results suggest that prophage infection of SDSE is somewhat restricted, resulting in a smaller number of virulence factors located in the prophage regions of SDSE
Other genome-encoded superantigen genes for mitogenic exotoxin Z, which are present in GAS [37], were not found in the GGS_124 genome. (iii) Proteases We found that a putative proteinase (SDEG_1906) and streptococcal C5a peptidase (SDEG_0933) [38] were conserved among GGS_124 and 5 closely related species
Summary
Streptococcus dysgalactiae subsp. equisimilis (SDSE) causes invasive streptococcal infections, including streptococcal toxic shock syndrome (STSS), as does Lancefield group A Streptococcus pyogenes (GAS). Equisimilis (SDSE) causes invasive streptococcal infections, including streptococcal toxic shock syndrome (STSS), as does Lancefield group A Streptococcus pyogenes (GAS). We sequenced the entire genome of SDSE strain GGS_124 isolated from a patient with STSS. Of 313 strains of GCS and GGS isolated from clinical samples in Southern India between 2006 and 2007, 254 (81.1%) were SDSE [9], as were 80% of the 266 invasive non-A and non-B b-hemolytic streptococcal isolates in the USA [3]. The spectrum and clinical courses of SDSE infection, including pharyngitis, cellulitis, infective arthritis, vertebral osteomyelitis, and streptococcal toxic shock syndrome (STSS), show substantial overlap with those of GAS [10,11,12,13,14,15,16]. We describe here the entire genome sequence of a Lancefield group G SDSE strain, GGS_124, which had been isolated from a patient with STSS
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