Abstract
Streptococcus dysgalactiae subsp. dysgalactiae (SDSD) has been considered a strict animal pathogen. Nevertheless, the recent reports of human infections suggest a niche expansion for this subspecies, which may be a consequence of the virulence gene acquisition that increases its pathogenicity. Previous studies reported the presence of virulence genes of Streptococcus pyogenes phages among bovine SDSD (collected in 2002–2003); however, the identity of these mobile genetic elements remains to be clarified. Thus, this study aimed to characterize the SDSD isolates collected in 2011–2013 and compare them with SDSD isolates collected in 2002–2003 and pyogenic streptococcus genomes available at the National Center for Biotechnology Information (NCBI) database, including human SDSD and S. dysgalactiae subsp. equisimilis (SDSE) strains to track temporal shifts on bovine SDSD genotypes. The very close genetic relationships between humans SDSD and SDSE were evident from the analysis of housekeeping genes, while bovine SDSD isolates seem more divergent. The results showed that all bovine SDSD harbor Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas IIA system. The widespread presence of this system among bovine SDSD isolates, high conservation of repeat sequences, and the polymorphism observed in spacer can be considered indicators of the system activity. Overall, comparative analysis shows that bovine SDSD isolates carry speK, speC, speL, speM, spd1, and sdn virulence genes of S. pyogenes prophages. Our data suggest that these genes are maintained over time and seem to be exclusively a property of bovine SDSD strains. Although the bovine SDSD genomes characterized in the present study were not sequenced, the data set, including the high homology of superantigens (SAgs) genes between bovine SDSD and S. pyogenes strains, may indicate that events of horizontal genetic transfer occurred before habitat separation. All bovine SDSD isolates were negative for genes of operon encoding streptolysin S, except for sagA gene, while the presence of this operon was detected in all SDSE and human SDSD strains. The data set of this study suggests that the separation between the subspecies “dysgalactiae” and “equisimilis” should be reconsidered. However, a study including the most comprehensive collection of strains from different environments would be required for definitive conclusions regarding the two taxa.
Highlights
Streptococcus dysgalactiae (SD) includes two subspecies: S. dysgalactiae subsp. dysgalactiae (SDSD) and S. dysgalactiae subsp. equisimilis (SDSE) (Jensen and Kilian, 2012)
Sequence analysis of the rRNA 16S from bovine SDSD isolates showed between 99.2% and 100% nucleotide identity to SDSD ATCC 2795, SDSD NCTC4670, SDSD NCTC13731, and SDSD NCTC4669 strains deposited in the National Center for Biotechnology Information (NCBI) Nucleotide database
The phylogeny of S. canis, S. dysgalactiae, Streptococcus equi, and S. pyogenes species based on Multilocus Sequence Analysis (MLSA) was reconstructed according to this analysis; S. dysgalactiae includes two separate clusters corresponding to the “dysgalactiae” and “equisimilis” subspecies (Jensen and Kilian, 2012)
Summary
Streptococcus dysgalactiae (SD) includes two subspecies: S. dysgalactiae subsp. dysgalactiae (SDSD) and S. dysgalactiae subsp. equisimilis (SDSE) (Jensen and Kilian, 2012). While SDSE has been recognized as an increasingly important human pathogen, SDSD has been considered a strictly animal pathogen and is commonly associated with bovine mastitis (Zadoks et al, 2011; Rato et al, 2013). Though the issue is not entirely clear-cut, the most likely scenario is that the species tree has S. dysgalactiae and S. pyogenes as sister species and, together with S. canis, establishes a very closely related branch. These data suggest that they have recently descended from a common ancestor (Suzuki et al, 2011; Jensen and Kilian, 2012; Lefébure et al, 2012). The MGEs are self-transmissible elements that are omnipresent in bacteria, harboring genes responsible for their maintenance, regulation, and mobility and genes encoding antimicrobial resistance, as well as other determinants, such as genes that encode virulence factors (Grohmann et al, 2003; McNeilly and McMillan, 2014)
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