Shigella sonnei.
Ontology highlight
ABSTRACT:
SUBMITTER: Torraca V
PROVIDER: S-EPMC7611039 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Shigella sonnei UCN59, isolated during an outbreak of S. sonnei in January 2007, was resistant to azithromycin (MIC 64 mg/L). The isolate contained a plasmid-borne mph(A) gene encoding a macrolide 2 -phosphotransferase that inactivates macrolides. Emergence of the mph(A) gene in S. sonnei may limit usefulness of azithromycin for treatment of shigellosis.
| S-EPMC2600399 | biostudies-literature
Project description:Shigella sonnei is the emerging pathogen globally, as it is the second common infectious species of shigellosis (bloody diarrhoea) in low- and middle-income countries (LMICs) and the leading one in developed world. The multifactorial processes and novel mechanisms have been identified in S. sonnei, that are collectively playing apart a substantial role in increasing its prevalence, while replacing the S. flexneri and other Gram-negative gut pathogens niche occupancy. Recently, studies suggest that due to improvement in sanitation S. sonnei has reduced cross-immunization from Plesiomonas shigelliodes (having same O-antigen as S. sonnei) and also found to outcompete the two major species of Enterobacteriaceae family (Shigella flexneri and Escherichia coli), due to encoding of type VI secretion system (T6SS). This review aimed to highlight S. sonnei as an emerging pathogen in the light of recent research with pondering aspects on its epidemiology, transmission, and pathogenic mechanisms. Additionally, this paper aimed to review S. sonnei disease pattern and related complications, symptoms, and laboratory diagnostic techniques. Furthermore, the available treatment reigns and antibiotic-resistance patterns of S. sonnei are also discussed, as the ciprofloxacin and fluoroquinolone-resistant S. sonnei has already intensified the global spread and burden of antimicrobial resistance. In last, prevention and controlling strategies are briefed to limit and tackle S. sonnei and possible future areas are also explored that needed more research to unravel the hidden mysteries surrounding S. sonnei.
| S-EPMC7489455 | biostudies-literature
Project description:Expression of type III secretion system (TTSS), a major determinant of virulence in Shigella, is markedly inhibited in a deletion mutant (cpxA) of the CpxAR two-component sensor at the level of post-transcriptional processing of the second TTSS regulator, InvE. A novel mutant of rodZ, which encodes a cytoskeletal protein involved in maintaining the rod-shaped morphology of bacilli, was isolated in a screen for mutations that restored TTSS expression in a cpxA mutant. The rodZ mutants of Shigella sonnei efficiently expressed InvE at 30°C, a temperature at which expression is normally repressed through temperature-dependent post-transcriptional regulation. Consistent with a marked increase in invE mRNA stability in the rodZ mutant, purified RodZ strongly bound to an invE RNA probe. Functional domain mapping indicated that the RNA binding activity of RodZ was dependent on a short basic region (KRRKKR) and multimer formation. Electron microscopy revealed that RodZ multimers formed filamentous superstructures, similar to another bacterial cytoskeletal protein, MreB. Our results indicate that RodZ functions as a novel membrane-bound RNA binding protein that provides a scaffold for post-transcriptional regulation. Phenotypic analysis of deletion mutant for RNA binding protein RodZ. The mutants analyzed in this study are further described in Jiro Mitobe, Itaru Yanagihara, Kiyouhisa Ohnishi, Akira Ishihama and Haruo Watanabe 2010. Bacterial cytoskeleton RodZ regulates post-transcriptional processing of Shigella type III secretion system. EMBO-J ( in submission).
2011-03-31 | GSE21051 | GEO
Project description: Not available
| S-EPMC2725971 | biostudies-literature
Project description:BackgroundShigella spp. are Gram-negative intracellular pathogenic bacteria belonging to the family Enterobacteriaceae and can cause bacterial dysentery, a severe diarrheal disease. The pathophysiological impact of the Gram-negative bacteria is highly related to the composition and structural variability of lipopolysaccharides, the major lipoid components of the outer membrane. Out of the 114 genes involved in the lipopolysaccharide biosynthesis pathway, 47 genes are specific to Shigella spp. Changes in the specific genes can lead to loss of the O polysaccharide side chain, resulting in rough (R) type bacteria with increased sensitivity to temperature, or hydrophobic antibiotics. The formation of various different lipopolysaccharides or lipooligosaccharides has been observed previously in a mutant line showing altered biological properties, but the genetic background has not been investigated in detail.ResultsThe parental strain of the mutant line, Shigella sonnei 4303, was subjected to whole genome sequencing to gain a better insight into the structure and biosynthesis of lipopolysaccharides. The sequencing revealed a 4,546,505 bp long genome including chromosomal and plasmid DNA, and the lipopolysaccharide biosynthesis genes were also identified. A comparison of the genome was performed with the phylogenetically closely related, wild type, well characterized, highly virulent strain, S. sonnei 53G.ConclusionAnalysis of the lipopolysaccharide biosynthetic genes helped us to get more insight into the pathogenicity and virulence of the bacteria. The genome revealed high similarities with S. sonnei 53G, which can be used as a standard in characterizing the S. sonnei 4303's R-type isogenic derivatives.
| S-EPMC6201595 | biostudies-literature
Project description:Shigella flexneri is historically regarded as the primary agent of bacillary dysentery, yet the closely-related Shigella sonnei is replacing S. flexneri, especially in developing countries. The underlying reasons for this dramatic shift are mostly unknown. Using a zebrafish (Danio rerio) model of Shigella infection, we discover that S. sonnei is more virulent than S. flexneri in vivo. Whole animal dual-RNAseq and testing of bacterial mutants suggest that S. sonnei virulence depends on its O-antigen oligosaccharide (which is unique among Shigella species). We show in vivo using zebrafish and ex vivo using human neutrophils that S. sonnei O-antigen can mediate neutrophil tolerance. Consistent with this, we demonstrate that O-antigen enables S. sonnei to resist phagolysosome acidification and promotes neutrophil cell death. Chemical inhibition or promotion of phagolysosome maturation respectively decreases and increases neutrophil control of S. sonnei and zebrafish survival. Strikingly, larvae primed with a sublethal dose of S. sonnei are protected against a secondary lethal dose of S. sonnei in an O-antigen-dependent manner, indicating that exposure to O-antigen can train the innate immune system against S. sonnei. Collectively, these findings reveal O-antigen as an important therapeutic target against bacillary dysentery, and may explain the rapidly increasing S. sonnei burden in developing countries.
2019-11-19 | GSE140544 | GEO
Project description:Shigella sonnei Genome sequencing and assembly
| PRJNA300887 | ENA
Project description:global fluoroquinolone resistant Shigella sonnei genomic study
| PRJNA320210 | ENA