Dataset Information

Clinical Manifestations and Bacterial Genomic Analysis of Group A Streptococcus Strains That Cause Pediatric Toxic Shock Syndrome.

ABSTRACT: We report here 18 cases of pediatric group A streptococcal toxic shock syndrome, associated clinical findings, and bacterial molecular genetic characteristics discovered through whole-genome sequencing. This comparative whole-genome sequencing revealed unique gene content (speK) and polymorphisms (dpiB) in emm87 group A Streptococcus, the relative contributions of which, in combination with the host response, in the development of streptococcal toxic shock syndrome remain to be elucidated.

SUBMITTER: Deniskin R

PROVIDER: S-EPMC6601382 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Clinical Manifestations and Bacterial Genomic Analysis of Group A Streptococcus Strains That Cause Pediatric Toxic Shock Syndrome.

Deniskin Roman R Shah Brittany B Muñoz Flor M FM Flores Anthony R AR

Journal of the Pediatric Infectious Diseases Society 20190701 3

We report here 18 cases of pediatric group A streptococcal toxic shock syndrome, associated clinical findings, and bacterial molecular genetic characteristics discovered through whole-genome sequencing. This comparative whole-genome sequencing revealed unique gene content (speK) and polymorphisms (dpiB) in emm87 group A Streptococcus, the relative contributions of which, in combination with the host response, in the development of streptococcal toxic shock syndrome remain to be elucidated. ...[more]

PMID: 30085250

Similar Datasets

Project description:BackgroundStreptococcus suis serotype 2 (S. suis 2, SS2) is a major zoonotic pathogen that causes only sporadic cases of meningitis and sepsis in humans. Most if not all cases of Streptococcal toxic shock syndrome (STSS) that have been well-documented to date were associated with the non-SS2 group A streptococcus (GAS). However, a recent large-scale outbreak of SS2 in Sichuan Province, China, appeared to be caused by more invasive deep-tissue infection with STSS, characterized by acute high fever, vascular collapse, hypotension, shock, and multiple organ failure.Methods and findingsWe investigated this outbreak of SS2 infections in both human and pigs, which took place from July to August, 2005, through clinical observation and laboratory experiments. Clinical and pathological characterization of the human patients revealed the hallmarks of typical STSS, which to date had only been associated with GAS infection. Retrospectively, we found that this outbreak was very similar to an earlier outbreak in Jiangsu Province, China, in 1998. We isolated and analyzed 37 bacterial strains from human specimens and eight from pig specimens of the recent outbreak, as well as three human isolates and two pig isolates from the 1998 outbreak we had kept in our laboratory. The bacterial isolates were examined using light microscopy observation, pig infection experiments, multiplex-PCR assay, as well as restriction fragment length polymorphisms (RFLP) and multiple sequence alignment analyses. Multiple lines of evidence confirmed that highly virulent strains of SS2 were the causative agents of both outbreaks.ConclusionsWe report, to our knowledge for the first time, two outbreaks of STSS caused by SS2, a non-GAS streptococcus. The 2005 outbreak was associated with 38 deaths out of 204 documented human cases; the 1998 outbreak with 14 deaths out of 25 reported human cases. Most of the fatal cases were characterized by STSS; some of them by meningitis or severe septicemia. The molecular mechanisms underlying these human STSS outbreaks in human beings remain unclear and an objective for further study.

Project description:BACKGROUND: Streptococcus 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. RESULTS: We 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. CONCLUSION: Genome 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.

Dataset Information

Clinical Manifestations and Bacterial Genomic Analysis of Group A Streptococcus Strains That Cause Pediatric Toxic Shock Syndrome.

Publications

Clinical Manifestations and Bacterial Genomic Analysis of Group A Streptococcus Strains That Cause Pediatric Toxic Shock Syndrome.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets