Azithromycin resistant Salmonella typhi in Nepal
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB37899 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4042541_1.fastq.gz | Fastqsanger.gz | |||
| ERR4042541_2.fastq.gz | Fastqsanger.gz | |||
| ERR4042542_1.fastq.gz | Fastqsanger.gz | |||
| ERR4042542_2.fastq.gz | Fastqsanger.gz | |||
| ERR4042543_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:BackgroundTyphoid fever remains a significant cause of morbidity and mortality in Asia and Africa. The emergence of azithromycin resistance in South Asia is concerning, as azithromycin is one of the last effective oral drugs for treating typhoid.ObjectivesTo describe the molecular mechanism and phylogenetics of azithromycin-resistant (AzithR) Salmonella Typhi isolates from Patan Hospital, Kathmandu, Nepal.MethodsWhole-genome sequences of three AzithR S. Typhi isolates (MIC >256 mg/L) were analysed and compared with a global collection to investigate the azithromycin resistance mechanism and phylogenetic structure. Clinical information is reported for one of the three patients infected with AzithR S. Typhi.ResultsThe three AzithR isolates belonged to the H58 lineage and were genetically identical; they were distantly related to contemporaneous S. Typhi from Nepal and AzithR S. Typhi recently described in Bangladesh. Azithromycin resistance was mediated by a non-synonymous mutation in the acrB gene (R717L). The three AzithR isolates showed reduced susceptibility to ciprofloxacin (double mutation in the gyrA: S83F and D87G), and were susceptible to ampicillin, chloramphenicol and co-trimoxazole. Clinical information from one patient suggested non-response to azithromycin treatment.ConclusionsThis is the first molecular description of AzithR S. Typhi in Nepal. These organisms showed no phylogenetic link to AzithR S. Typhi in Bangladesh. Our data suggest that increasing use of azithromycin may pose a strong selective pressure driving the emergence of AzithR S. Typhi in South Asia. Further investigations are needed to evaluate treatment responses to azithromycin, predict evolutionary trajectories, and track the transmission of these organisms.
| S-EPMC8210228 | biostudies-literature
Project description:This study describes how Salmonella Typhi, the pathogen responsible for typhoid fever, uses similar strategies to escape immune defense responses and survive within its human host. To elucidate the early mechanisms of typhoid fever, we performed studies using healthy human intestinal tissue samples to analyze gene expression changes in human intestinal specimens and bacterial cells both separately and after colonization. Our results showed mechanistic strategies that S. Typhi uses to rearrange the cellular machinery of the host cytoskeleton to successfully invade the intestinal epithelium, promote polarized cytokine release and evade immune system activation by downregulating genes involved in antigen sampling and presentation during infection.
2018-06-15 | GSE113333 | GEO
Project description:Six sequencing libraries was prepared from S. Typhi planktonic cells and biofilm cells using Illumina HiSeq 2500 sequencing to investigate differential gene expression between the two conditions. The transcriptome was processed using Cufflinks and there were a total of 35 up-regulated genes and 29 down-regulated genes log2-fold change values of greater than 2 and less than negative 2. The differentially expressed genes were identified using BLAST and the functions was analysed. This study provides an overview of the genes that are differentially expressed in S. Typhi when it transitions from the planktonic to the biofilm phenotype. The data will provide a basis for further study is necessary to uncover the mechanisms of biofilm formation in S. Typhi and discovery of novel gene functions or pathways associated with the development of the typhoid carrier state. This data may also be used to elucidate the effect of biofilm on the virulence and pathogenicity of S. Typhi in chronic carriers.
2017-10-31 | GSE93686 | GEO
Project description:Human genetic diversity can reveal critical factors in host-pathogen interactions. This is especially useful for human-restricted pathogens like Salmonella enterica serovar Typhi (S. Typhi), the cause of Typhoid fever. One key dynamic during infection is competition for nutrients: host cells attempt to restrict intracellular replication by depriving bacteria of key nutrients or delivering toxic metabolites in a process called nutritional immunity. Here, a cellular genome-wide association study of intracellular replication by S. Typhi in nearly a thousand cell lines from around the world—and extensive follow-up using intracellular S. Typhi transcriptomics and manipulation of magnesium concentrations—demonstrates that the divalent cation channel mucolipin-2 (MCOLN2) restricts S. Typhi intracellular replication through magnesium deprivation. Our results reveal natural diversity in Mg2+ limitation as a key component of nutritional immunity against S. Typhi.
2023-01-05 | GSE222194 | GEO
Project description:Global travel has led to intermittent importation of multidrug-resistant Salmonella enterica serovar Typhi into industrialized countries. We detected azithromycin-resistant Salmonella Typhi in Singapore, of which 2 isolates were likely locally acquired. Ongoing vigilance and surveillance to minimize the public health risk for this serious pathogen is needed.
| S-EPMC7853538 | biostudies-literature
Project description:Transcriptional profiling of three sequenced S. enterica strains: S. Typhimurium LT2, S. Typhi CT18, and S. Typhi Ty2 in PhoP-inducing and non-inducing conditions in vitro, and compared these results to profiles of phoP-/Q- mutants derived from S. Typhimurium LT2 and S. Typhi Ty2.
2009-08-19 | GSE17670 | GEO
Project description:Salmonella enterica serovar Typhi (S. Typhi), a human-restricted pathogen, enters the host through the gut to cause typhoid fever. Recent calculations of the typhoid fever burden estimated that more than 20 million new typhoid fever cases occur in low and middle-income countries, resulting in 129,000-223,000 deaths yearly. Interestingly, upon the resolution of acute disease, 1%-5% of patients become asymptomatic chronic carriers of S. Typhi. Chronically infected hosts are not only critical reservoirs of infection that transmit the disease to naive individuals but are also predisposed to developing gallbladder carcinoma (GBC). Nevertheless, the molecular mechanisms involved in the early interactions between gallbladder epithelial cells and S. Typhi remain largely unknown. Based on our previous studies showing that very closely related S. Typhi strains elicit distinct innate immune responses, we hypothesized that host molecular pathways activated by S. Typhi strains derived from acutely and chronically infected patients will differ. To test this hypothesis, we used a novel human organoid-derived polarized gallbladder monolayer (HODGM) model, and 13 S. Typhi strains derived from acutely (n=6) and chronically (n=7) infected patients. We found that S. Typhi strains derived from acutely and chronically infected patients differentially regulate mitogen-activated protein kinase (MAPK) and S6 transcription factors. This differential regulation impacts, at least in part, the cytokine signaling pathway involved in the production of TNF- and IL-6 and is likely to play a critical role in inducing chronic S. Typhi infection in the gallbladder.
2024-04-05 | GSE253700 | GEO
Project description:Ceftriaxone resistant H58 Salmonella Typhi
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Project description:Macrophages provide a crucial environment for Salmonella enterica serovar Typhi (S. Typhi) to multiply during typhoid fever, yet our understanding of how human macrophages and S. Typhi interact remains limited. In this study, we delve into the dynamics of S. Typhi replication within human macrophages and the resulting heterogeneous transcriptomic responses of macrophages during infection. Our study reveals key factors that influence macrophage diversity, uncovering distinct immune and metabolic pathways associated with different stages of S. Typhi intracellular replication in macrophages. Of note, we found that macrophages harboring replicating S. Typhi are skewed towards an M1 pro-inflammatory state, whereas macrophages containing non-replicating S. Typhi exhibit neither a distinct M1 pro-inflammatory nor M2 anti-inflammatory state. Additionally, macrophages with replicating S. Typhi were characterized by the increased expression of genes associated with STAT3 phosphorylation and the activation of the STAT3 transcription factor. Our results shed light on transcriptomic pathways involved in the susceptibility of human macrophages to intracellular S. Typhi replication, thereby providing crucial insight into host phenotypes that restrict and support S. Typhi infection.
2024-05-20 | GSE267899 | GEO
Project description:S. Typhi was cultured in broth, diluted and resuspended in water. RNA was prepared from the original broth culture (control), and from S. Typhi suspended in water for 0.5, 6 and 24 hours incubated at 28c without shaking
2018-09-07 | E-MTAB-7160 | biostudies-arrayexpress