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PROVIDER: PRJNA335742 | ENA |
REPOSITORIES: ENA
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Project description:Group C Streptococcus dysgalactiae subsp. dysgalactiae (GCS) field strains causative of bovine mastitis and group C or group G Streptococcus dysgalactiae subsp. equisimilis (GCS/GGS) isolates from human infections were tested for the presence of virulence genes employing a microarray containing 220 virulence genes of S. pyogenes (GAS).
2011-05-05 | E-MEXP-3168 | biostudies-arrayexpress
Project description:Streptococcus dysgalactiae subsp. equisimilis Genome Diversity
| PRJNA327242 | ENA
Project description:Streptococcus dysgalactiae subsp. equisimilis
| PRJEB43000 | ENA
Project description:Streptococcus dysgalactiae subsp. equeisimilis (SDSE) has Lancefield group G or C antigens. Recent epidemiological studies reveal that invasive SDSE infections have been increasing in Asia, Europe and US. Although SDSE possesses similar virulence factors to S. pyogenes including streptolysin S (SLS) and streptolysin O (SLO), some important S. pyogenes virulence factors including active superantigens, SpeB and a hyarulonic acids capsule are missing in SDSE genome. The mechanisms and the key virulence factors for causing invasive diseases by SDSE are poorly understood. Here, we analyzed the transcriptome of SDSE in vivo using the murine sepsis model, revealing the strategy of SDSE to destruct host tissues with the virulence factors and to scavenge depleted nutrients. The expression of SLO operon increased at relatively early stage of infection while the SLS and hyaluronidases upregulated after 4h post infection. Microarray data suggested that SDSE degraded host tissue polysaccharides by streptococcal-secreting poly/oligosaccharide lyases and simultaneously used the Entner-Doudoroff pathway to metabolize acquired carbohydrates. A global negative virulence gene regulator CsrRS of SDSE modulated the expressions of genes encoding SLS and the carbohydrate metabolism enzymes. Moreover, csrS deficient mutant induced sever systemic hemolysis in mice. The most frequently isolated stG6792 strains from invasive disease secreted abundant SLS and SLO rather than other SDSE emm types, indicating the relationship between the SLS and SLO productions and poor outcome by the stG6792 strain infection. Our findings suggest that the concomitant regulation of virulence factors destructing the host tissues and metabolic enzymes play an important role to produce invasive diseases by SDSE. To analyze gene expressions in group G streptococci with the murine infection model, we developed a custom microarray for Streptococcus dysgalactiae subsp. equisimilis (SDSE) based on the genome sequences of three SDSE strains; GGS_124, ATCC12923 and RE378. We intraperitoneally inoculated 10^8 CFU of GGS_124 stain and the csrS deficient mutant into ddY mice. Bacterial cells were collected from the abdominal cavity at 0, 2, 4 and 8 h post infection. GGS_124 cells were also collected from OD600=0.6 culture in brain heart infusion broth as a control.
2013-09-09 | E-GEOD-43222 | biostudies-arrayexpress
Project description:Streptococcus dysgalactiae subspecies equisimilis (SDSE) is a Gram-positive bacterial pathogen that infects humans and is closely related to group A streptococcus (GAS). Compared to GAS, far less is known about SDSE pathobiology. Increased rates of invasive SDSE infections have recently been reported in many countries. One SDSE emm type, stG62647, is known to cause severe diseases, including necrotizing soft-tissue infections, endocarditis, and osteoarticular infections. To increase our understanding of the molecular pathogenesis of stG62647 SDSE isolates causing human infections, we sequenced to closure the genomes of 120 stG62647 SDSE isolates. The genomes varied in size from 2.1 to 2.24 megabase pairs. Consistent with previous data, the great majority of stG62647 isolates had IS1548 integrated into the silB gene, thereby inactivating it. Regions of difference in gene content, including putative mobile genetic elements, were the largest source of genomic diversity. All 120 stG62647 isolates were assayed for virulence using a well-established mouse model of necrotizing myositis. An unexpectedly wide range of virulence was identified (20% to 95%), as assessed by near-mortality data. To explore the molecular mechanisms underlying virulence differences, we analyzed RNAseq transcriptome profiles for 38 stG62647 isolates (comprising the 19 least and most virulent) grown in vitro. Genetic polymorphisms were identified from whole-genome sequence data. Collectively, the results suggest that these SDSE isolates use multiple genetic pathways to achieve an altered virulence phenotype. Our study integrates genomic, mouse virulence, and RNAseq data to advance our understanding of SDSE pathobiology and its molecular pathogenesis.
2024-07-20 | GSE272047 | GEO
Project description:Streptococcus dysgalactiae subsp. equisimilis L1 genome sequencing
| PRJDA42151 | ENA
Project description:Streptococcus dysgalactiae subsp. equisimilis RE378 genome sequencing
| PRJDA34711 | ENA
Project description:Streptococcus dysgalactiae subsp. equisimilis Genome sequencing and assembly
| PRJNA552440 | ENA
Project description:Streptococcus dysgalactiae subsp. equisimilis Genome sequencing and assembly
| PRJNA811777 | ENA
Project description:Streptococcus dysgalactiae subsp. equisimilis Genome sequencing and assembly
| PRJNA657274 | ENA