scholarly journals Genomic characterization of the non-O1/non-O139 Vibrio cholerae strain that caused a gastroenteritis outbreak in Santiago, Chile, 2018

2019 ◽  
Author(s):  
Mónica Arteaga ◽  
Juliana Velasco ◽  
Shelly Rodriguez ◽  
Maricel Vidal ◽  
Carolina Arellano ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Sequence Data ◽  
Genomic Islands ◽  
Cholerae Strain ◽  
Supplementary Data ◽  
Gastroenteritis Outbreak ◽  
Secretion Systems ◽  
Pathogenic Potential ◽  
Data Files

AbstractVibrio cholerae is a human pathogen, which is transmitted by the consumption of contaminated food or water. V. cholerae strains belonging to the serogroups O1 and O139 can cause cholera outbreaks and epidemics, a severe life-threatening diarrheal disease. In contrast, serogroups other than O1 and O139, denominated as non-O1/non-O139, have been mainly associated with sporadic cases of moderate or mild diarrhea, bacteremia and wound infections. Here we investigated the virulence determinants and phylogenetic origin of a non-O1/non-O139 V. cholerae strain that caused a gastroenteritis outbreak in Santiago, Chile, 2018. We found that this outbreak strain lacks the classical virulence genes harboured by O1 and O139 strains, including the cholera toxin (CT) and the toxin-coregulated pilus (TCP). However, this strain carries genomic islands (GIs) encoding Type III and Type VI secretion systems (T3SS/T6SS) and antibiotic resistance genes. Moreover, we found these GIs are wide distributed among several lineages of non-O1/non-O139 strains. Our results suggest that the acquisition of these GIs may enhance the virulence of non-O1/non-O139 strains that lack the CT and TCP-encoding genes. Our results highlight the pathogenic potential of these V. cholerae strains.DATA SUMMARYSequence data were submitted to GenBank under the accession number SRLP00000000. The authors confirm that all supporting data and protocols have been provided within the article or through supplementary data files.Data statementAll supporting data, code and protocols have been provided within the article or through supplementary data files. Four supplementary tables are available with the online version of this article.

scholarly journals Type III Secretion Is Essential for the Rapidly Fatal Diarrheal Disease Caused by Non-O1, Non-O139 Vibrio cholerae

mBio ◽  
2011 ◽  
Vol 2 (3) ◽  
Author(s):  
Ok S. Shin ◽  
Vincent C. Tam ◽  
Masato Suzuki ◽  
Jennifer M. Ritchie ◽  
Roderick T. Bronson ◽  
...  
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Intestinal Epithelium ◽  
Type Iii Secretion ◽  
Diarrheal Disease ◽  
Secretion Systems ◽  
Content Type ◽  
Type Iii ◽  
Severe Diarrhea ◽  
Toxin Coregulated Pilus

ABSTRACTCholera is a severe diarrheal disease typically caused by O1 serogroup strains ofVibrio cholerae. The pathogenicity of all pandemicV. choleraeO1 strains relies on two critical virulence factors: cholera toxin, a potent enterotoxin, and toxin coregulated pilus (TCP), an intestinal colonization factor. However, certain non-O1, non-O139V. choleraestrains, such as AM-19226, do not produce cholera toxin or TCP, yet they still cause severe diarrhea. The molecular basis for the pathogenicity of non-O1, non-O139V. choleraehas not been extensively characterized, but many of these strains encode related type III secretion systems (TTSSs). Here, we used infant rabbits to assess the contribution of the TTSS to non-O1, non-O139V. choleraepathogenicity. We found that all animals infected with wild-type AM-19226 developed severe diarrhea even more rapidly than rabbits infected withV. choleraeO1. UnlikeV. choleraeO1 strains, which do not damage the intestinal epithelium in rabbits or humans, AM-19226 caused marked disruptions of the epithelial surface in the rabbit small intestine. TTSS proved to be essential for AM-19226 virulence in infant rabbits; an AM-19226 derivative deficient for TTSS did not elicit diarrhea, colonize the intestine, or induce pathological changes in the intestine. Deletion of either one of the two previously identified or two newly identified AM-19226 TTSS effectors reduced but did not eliminate AM-19226 pathogenicity, suggesting that at least four effectors contribute to this strain’s virulence. In aggregate, our results suggest that the TTSS-dependent virulence in non-O1, non-O139V. choleraerepresents a new type of diarrheagenic mechanism.IMPORTANCECholera, which is caused byVibrio cholerae, is an important cause of diarrheal disease in many developing countries. The mechanisms of virulence of nonpandemic strains that can cause a diarrheal illness are poorly understood. AM-19226, like several other pathogenic, nonpandemicV. choleraestrains, carries genes that encode a type III secretion system (TTSS), but not cholera toxin (CT) or toxin coregulated pilus (TCP). In this study, we used infant rabbits to study AM-19226 virulence. Infant rabbits orally inoculated with this strain rapidly developed a fatal diarrheal disease, which was accompanied by marked disruptions of the intestinal epithelium. This strain’s TTSS proved essential for its pathogenicity, and there was no diarrhea, intestinal pathology, or colonization in rabbits infected with a TTSS mutant. The effector proteins translocated by the TTSS all appear to contribute to AM-19226 virulence. Thus, our study provides insight intoin vivomechanisms by which a novel TTSS contributes to diarrheal disease caused by nonpandemic strains ofV. cholerae.

scholarly journals Draft Genome Sequence of an Environmental Vibrio cholerae Strain, 2012Env-25, Obtained Using Nanopore Sequencing Technology

2020 ◽  
Vol 9 (32) ◽  
Author(s):  
V Lyju Jose ◽  
Matthew T. Pileggi ◽  
Meer Taifur Alam ◽  
Afsar Ali ◽  
Adam C. N. Wong
Keyword(s):  
Vibrio Cholerae ◽  
Genome Sequence ◽  
Bacterial Species ◽  
Draft Genome ◽  
Draft Genome Sequence ◽  
Cholerae Strain ◽  
Pathogenic Potential ◽  
Content Type ◽  
Oxford Nanopore ◽  
Oxford Nanopore Technologies

ABSTRACT Vibrio cholerae is a halophilic Gram-negative bacterial species and the etiological agent of cholera. Here, we report the draft genome sequence of an environmental V. cholerae strain, 2012Env-25, obtained using Oxford Nanopore Technologies (ONT) to provide insights into the ecology, evolution, and pathogenic potential of this bacterium.

scholarly journals Genomic characterization of the non-O1/non-O139 Vibrio cholerae strain that caused a gastroenteritis outbreak in Santiago, Chile, 2018

2020 ◽  
Vol 6 (3) ◽  
Author(s):  
Mónica Arteaga ◽  
Juliana Velasco ◽  
Shelly Rodriguez ◽  
Maricel Vidal ◽  
Carolina Arellano ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Cholerae Strain ◽  
Gastroenteritis Outbreak ◽  
Genomic Characterization

scholarly journals VCGIDB: A Database and Web Resource for the Genomic Islands from Vibrio cholerae

Pathogens ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 261
Author(s):  
YoungJae Hur ◽  
Mauricio Chalita ◽  
Sung-min Ha ◽  
Inwoo Baek ◽  
Jongsik Chun
Keyword(s):  
Vibrio Cholerae ◽  
Genomic Island ◽  
Diarrheal Disease ◽  
Prediction Method ◽  
Genomic Islands ◽  
Large Genome ◽  
Web Resource ◽  
Comprehensive Information ◽  
The World ◽  
Life Threatening

Vibrio cholerae is the causative agent of cholera, which is a severe, life-threatening diarrheal disease. The current seventh pandemic has not been eradicated and the outbreak is still ongoing around the world. The evolution of the pandemic-causing strain has been greatly influenced by lateral gene transfer, and the mechanisms of acquisition of pathogenicity in V. cholerae are mainly involved with genomic islands (GIs). Thus, detecting GIs and their comprehensive information is necessary to understand the continuing resurgence and newly emerging pathogenic V. cholerae strains. In this study, 798 V. cholerae strains were tested using the GI-Scanner algorithm, which was developed to detect candidate GIs and identify them in a comparative genomics approach. The algorithm predicted 435 highly possible genomic islands, and we built a database, called Vibrio cholerae Genomic Island Database (VCGIDB). This database shows advanced results that were acquired from a large genome set using phylogeny-based predictions. Moreover, VCGIDB is a highly expendable database that does not require intensive computation, which enables us to update it with a greater number of genomes using a novel genomic island prediction method. The VCGIDB website allows the user to browse the data and presents the results in a visual manner.

scholarly journals A Review on Diagnostic Methods for the Identification of Vibrio cholerae

2020 ◽  
pp. 136-164
Author(s):  
Tarh, Jacqueline Ebob
Keyword(s):  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Variable Number Tandem Repeat ◽  
Simultaneous Detection ◽  
Diagnostic Methods ◽  
Cholerae Strain ◽  
Low Resource Settings ◽  
Remote Areas ◽  
Low Resource ◽  
Life Threatening

The severe diarrheal disease Cholera, has gained public health importance because of its life-threatening effect. The detection of the causative agent of this disease (Vibrio cholerae (V.  Cholerae) O1 or O139) from a specimen (stool, vomitus of food sample) remains a major concern in the world today. Phenotypic finger printing (the conventional methods) of the toxigenic V. cholerae strain, remains the gold standard for the laboratory diagnosis of cholera; especially during cholera epidemic outbreaks. Detection around the remote areas which are usually rampaged by these outbreaks is usually difficult due to lack of required diagnostic facilities in small laboratories. However, the use of phenotypic approaches have some major setbacks as they are usually labor-intensive and time consuming. This delays treatment commencement especially in life threatening cases.To alleviate these setbacks, rapid molecular typing techniques involving the Polymerase chain reaction (PCR) amplification, hybridization methods, Pulsed Field Gel Electrophoresis (PFGE), Multilocus Sequence Typing (MLST), Multiple-Locus Variable Number Tandem Repeat Analysis (MVLA), Fluorescent Amplified Fragment Length Polymorphism (FAFLP),  Whole Genome Sequencing (WGS) etc. represent promising tools for early detection of the pathogen V. cholerae O1/O139 even in remote areas where laboratory resources are poor. Immunoassay-based techniques like enzyme-linked immune-sorbent assay (ELISA), coagglutination, immunofluorescence, and quartz crystal microbalance (QCM), are capital/labour intensive and expensive for low resource settings. Rapid diagnostic tests based on immune-chromatography principle have also been developed for simultaneous detection of V. choleraesero groups O1 and O139. These test kits are easy to use, transport, and fast. All these methods enable the subtyping of unrelated bacterial strains and they all operate with different accuracies, discriminatory ability, and reproducibility. This review sought to address some of the methods used in diagnosing the disease cholera, with the objective of identifying the best and easiest of the methods that can help to curb the cholera problem (deaths) often encountered, especially in low resource settings in the developing countries (Nigeria inclusive).

scholarly journals Dominant Vibrio cholerae phage exhibits lysis inhibition sensitive to disruption by a defensive phage satellite

2019 ◽  
Author(s):  
Stephanie G. Hays ◽  
Kimberley D. Seed
Keyword(s):  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Single Cells ◽  
Bacterial Genome ◽  
Genomic Islands ◽  
Phage Infection ◽  
Etiological Agent ◽  
Clinical Samples ◽  
Host Bacterium ◽  
Lysis Inhibition

AbstractBacteriophages and their bacterial hosts are locked in a dynamic evolutionary arms race. Phage satellites, selfish genomic islands which exploit both host bacterium and target phage, further complicate the evolutionary fray. One such tripartite system involves the etiological agent of the diarrheal disease cholera – Vibrio cholerae, the predominant phage isolated from cholera patients – ICP1, and a phage satellite – PLE. When ICP1 infects V. cholerae harboring the integrated PLE genome, PLE accelerates host lysis, spreading the PLE while completely blocking phage production protecting V. cholerae at the population level. Here we identify a single PLE gene, lidI, sufficient to mediate accelerated lysis during ICP1 infection and demonstrate that LidI functions through disrupting lysis inhibition – an understudied outcome of phage infection when phages vastly outnumber their hosts. This work identifies ICP1-encoded holin and antiholin genes teaA and arrA respectively, that mediate this first example of lysis inhibition outside the T-even coliphages. Through lysis inhibition disruption, LidI is sufficient to limit the number of progeny phage produced from an infection. Consequently, this disruption bottlenecks ICP1 evolution as probed by recombination and CRISPR-Cas targeting assays. These studies link novel characterization of the classic phenomenon of lysis inhibition with a conserved protein in a dominant phage satellite, highlighting the importance of lysis timing during infection and parasitization, as well as providing insight into the populations, relationships, and evolution of bacteria, phages, and phage satellites in nature.ImportanceWith increasing awareness of microbiota impacting human health comes intensified examination of, not only bacteria and the bacteriophages that prey upon them, but also the mobile genetic elements (MGEs) that mediate interactions between them. Research is unveiling evolutionary strategies dependent on sensing the milieu: quorum sensing impacts phage infection, phage teamwork overcomes bacterial defenses, and abortive infections sacrifice single cells protecting populations. Yet, the first discovered environmental sensing by phages, known as lysis inhibition (LIN), has only been studied in the limited context of T-even coliphages. Here we characterize LIN in the etiological agent of the diarrheal disease cholera, Vibrio cholerae, infected by a phage ubiquitous in clinical samples. Further, we show that a specific MGE, the phage satellite PLE, collapses LIN with a conserved protein during its anti-phage program. The insights gleaned from this work add to our expanding understanding of microbial fitness in natural contexts beyond the canonical bacterial genome and into the realm of antagonistic evolution driven by phages and satellites.

scholarly journals Phylogenomic analysis of Clostridioides difficile ribotype 106 strains reveals novel genetic islands and emergent phenotypes

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bryan Angelo P. Roxas ◽  
Jennifer Lising Roxas ◽  
Rachel Claus-Walker ◽  
Anusha Harishankar ◽  
Asad Mansoor ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Diarrheal Disease ◽  
The United States ◽  
Genomic Islands ◽  
Rapid Expansion ◽  
Phylogenomic Analysis ◽  
Community Settings ◽  
Hamster Model ◽  
Clostridioides Difficile ◽  
Healthcare Associated

AbstractClostridioides difficile infection (CDI) is a major healthcare-associated diarrheal disease. Consistent with trends across the United States, C. difficile RT106 was the second-most prevalent molecular type in our surveillance in Arizona from 2015 to 2018. A representative RT106 strain displayed robust virulence and 100% lethality in the hamster model of acute CDI. We identified a unique 46 KB genomic island (GI1) in all RT106 strains sequenced to date, including those in public databases. GI1 was not found in its entirety in any other C. difficile clade, or indeed, in any other microbial genome; however, smaller segments were detected in Enterococcus faecium strains. Molecular clock analyses suggested that GI1 was horizontally acquired and sequentially assembled over time. GI1 encodes homologs of VanZ and a SrtB-anchored collagen-binding adhesin, and correspondingly, all tested RT106 strains had increased teicoplanin resistance, and a majority displayed collagen-dependent biofilm formation. Two additional genomic islands (GI2 and GI3) were also present in a subset of RT106 strains. All three islands are predicted to encode mobile genetic elements as well as virulence factors. Emergent phenotypes associated with these genetic islands may have contributed to the relatively rapid expansion of RT106 in US healthcare and community settings.

scholarly journals MetR-Regulated Vibrio cholerae Metabolism Is Required for Virulence

mBio ◽  
2012 ◽  
Vol 3 (5) ◽  
Author(s):  
Ryan W. Bogard ◽  
Bryan W. Davies ◽  
John J. Mekalanos
Keyword(s):  
Amino Acid ◽  
Vibrio Cholerae ◽  
Virulence Factor ◽  
Current Knowledge ◽  
Intestinal Colonization ◽  
Wild Type ◽  
Pathogenic Potential ◽  
Content Type ◽  
Mouse Intestine

ABSTRACTLysR-type transcriptional regulators (LTTRs) are the largest, most diverse family of prokaryotic transcription factors, with regulatory roles spanning metabolism, cell growth and division, and pathogenesis. Using a sequence-defined transposon mutant library, we screened a panel ofV. choleraeEl Tor mutants to identify LTTRs required for host intestinal colonization. Surprisingly, out of 38 LTTRs, only one severely affected intestinal colonization in the suckling mouse model of cholera: the methionine metabolism regulator, MetR. Genetic analysis of genes influenced by MetR revealed thatglyA1andmetJwere also required for intestinal colonization. Chromatin immunoprecipitation of MetR and quantitative reverse transcription-PCR (qRT-PCR) confirmed interaction with and regulation ofglyA1, indicating that misregulation ofglyA1is likely responsible for the colonization defect observed in themetRmutant. TheglyA1mutant was auxotrophic for glycine but exhibited wild-type trimethoprim sensitivity, making folate deficiency an unlikely cause of its colonization defect. MetJ regulatory mutants are not auxotrophic but are likely altered in the regulation of amino acid-biosynthetic pathways, including those for methionine, glycine, and serine, and this misregulation likely explains its colonization defect. However, mutants defective in methionine, serine, and cysteine biosynthesis exhibited wild-type virulence, suggesting that these amino acids can be scavenged in vivo. Taken together, our results suggest that glycine biosynthesis may be required to alleviate an in vivo nutritional restriction in the mouse intestine; however, additional roles for glycine may exist. Irrespective of the precise nature of this requirement, this study illustrates the importance of pathogen metabolism, and the regulation thereof, as a virulence factor.IMPORTANCEVibrio choleraecontinues to be a severe cause of morbidity and mortality in developing countries. Identification ofV. choleraefactors critical to disease progression offers the potential to develop or improve upon therapeutics and prevention strategies. To increase the efficiency of virulence factor discovery, we employed a regulator-centric approach to multiplex our in vivo screening capabilities and allow whole regulons inV. choleraeto be interrogated for pathogenic potential. We identified MetR as a new virulence regulator and serine hydroxymethyltransferase GlyA1 as a new MetR-regulated virulence factor, both required byV. choleraeto colonize the infant mouse intestine. Bacterial metabolism is a prerequisite to virulence, and current knowledge of in vivo metabolism of pathogens is limited. Here, we expand the known role of amino acid metabolism and regulation in virulence and offer new insights into the in vivo metabolic requirements ofV. choleraewithin the mouse intestine.

scholarly journals Pathogenic Potential of Environmental Vibrio cholerae Strains Carrying Genetic Variants of the Toxin-Coregulated Pilus Pathogenicity Island

2003 ◽  
Vol 71 (2) ◽  
pp. 1020-1025 ◽  
Author(s):  
Shah M. Faruque ◽  
M. Kamruzzaman ◽  
Ismail M. Meraj ◽  
Nityananda Chowdhury ◽  
G. Balakrish Nair ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Genetic Variants ◽  
Pathogenicity Island ◽  
Biologically Active ◽  
Pathogenic Potential ◽  
Origin And Evolution ◽  
Colonization Factor ◽  
Evolution Of Virulence ◽  
Toxin Coregulated Pilus ◽  
El Tor

ABSTRACT The major virulence factors of toxigenic Vibrio cholerae are cholera toxin (CT), which is encoded by a lysogenic bacteriophage (CTXΦ), and toxin-coregulated pilus (TCP), an essential colonization factor which is also the receptor for CTXΦ. The genes for the biosynthesis of TCP are part of a larger genetic element known as the TCP pathogenicity island. To assess their pathogenic potential, we analyzed environmental strains of V. cholerae carrying genetic variants of the TCP pathogenicity island for colonization of infant mice, susceptibility to CTXΦ, and diarrheagenicity in adult rabbits. Analysis of 14 environmental strains, including 3 strains carrying a new allele of the tcpA gene, 9 strains carrying a new allele of the toxT gene, and 2 strains carrying conventional tcpA and toxT genes, showed that all strains colonized infant mice with various efficiencies in competition with a control El Tor biotype strain of V. cholerae O1. Five of the 14 strains were susceptible to CTXΦ, and these transductants produced CT and caused diarrhea in adult rabbits. These results suggested that the new alleles of the tcpA and toxT genes found in environmental strains of V. cholerae encode biologically active gene products. Detection of functional homologs of the TCP island genes in environmental strains may have implications for understanding the origin and evolution of virulence genes of V. cholerae.

scholarly journals Systematic Identification of Cyclic-di-GMP Binding Proteins in Vibrio cholerae Reveals a Novel Class of Cyclic-di-GMP-Binding ATPases Associated with Type II Secretion Systems

2015 ◽  
Vol 11 (10) ◽  
pp. e1005232 ◽  
Author(s):  
Kevin G. Roelofs ◽  
Christopher J. Jones ◽  
Sarah R. Helman ◽  
Xiaoran Shang ◽  
Mona W. Orr ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Binding Proteins ◽  
Type Ii Secretion ◽  
Type Ii ◽  
Secretion Systems ◽  
Systematic Identification
Sign in / Sign up

Export Citation Format

Share Document