scholarly journals Recent Vibrio cholerae O1 Epidemic Strains Are Unable To Replicate CTXΦ Prophage Genome

mSphere ◽  
2021 ◽  
Author(s):  
Kaoru Ochi ◽  
Tamaki Mizuno ◽  
Prosenjit Samanta ◽  
Asish K. Mukhopadhyay ◽  
Shin-ichi Miyoshi ◽  
...  
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Content Type ◽  
Ctxφ Prophage ◽  
Vibrio Cholerae O1 ◽  
El Tor

Cholera is an acute diarrheal disease caused by pathogenic strains of V. cholerae generated by lysogenization of the filamentous cholera toxin phage CTXΦ. The analysis revealed that recent isolates possessed altered CTXΦ prophage array of prototype El Tor strain and were defective in replicating the CTXΦ genome.

scholarly journals A Quinazoline-2,4-Diamino Analog Suppresses Vibrio cholerae Flagellar Motility by Interacting with Motor Protein PomB and Induces Envelope Stress

2013 ◽  
Vol 57 (8) ◽  
pp. 3950-3959 ◽  
Author(s):  
Hongxia Wang ◽  
Li Zhang ◽  
Anisia J. Silva ◽  
Jorge A. Benitez
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Motor Protein ◽  
Polar Flagellum ◽  
Flagellar Motility ◽  
Extracellular Rna ◽  
Content Type ◽  
Envelope Stress ◽  
Causative Agents ◽  
El Tor

ABSTRACTVibrio choleraestrains of serogroups O1 and O139, the causative agents of the diarrheal illness cholera, express a single polar flagellum powered by sodium motive force and require motility to colonize and spread along the small intestine. In a previous study, we described a high-throughput assay for screening for small molecules that selectively inhibit bacterial motility and identified a family of quinazoline-2,4-diamino analogs (Q24DAs) that (i) paralyzed the sodium-driven polar flagellum ofVibriosand (ii) diminished cholera toxin secreted by El Tor biotypeV. cholerae. In this study, we provide evidence that a Q24DA paralyzes the polar flagellum by interacting with the motor protein PomB. Inhibition of motility with the Q24DA enhanced the transcription of the cholera toxin genes in both biotypes. We also show that the Q24DA interacts with outer membrane protein OmpU and other porins to induce envelope stress and expression of the extracellular RNA polymerase sigma factor σE. We suggest that Q24DA-induced envelope stress could affect the correct folding, assembly, and secretion of pentameric cholera toxin in El Tor biotypeV. choleraeindependently of its effect on motility.

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 Complete Genome Sequence of Vibrio cholerae O1 El Tor Strain C6706

2021 ◽  
Vol 10 (3) ◽  
Author(s):  
Yuding Weng ◽  
X. Renee Bina ◽  
James E. Bina
Keyword(s):  
Global Health ◽  
Vibrio Cholerae ◽  
Genome Sequence ◽  
Complete Genome Sequence ◽  
Human Disease ◽  
Complete Genome ◽  
Content Type ◽  
Health Threat ◽  
Vibrio Cholerae O1 ◽  
El Tor

ABSTRACT Vibrio cholerae is a global health threat and a model enteric pathogen that causes the human disease cholera. Here, we report the complete genome sequence of the seventh-pandemic V. cholerae O1 El Tor strain C6706.

scholarly journals Variation in Epitopes of the B Subunit of El Tor and Classical Biotype Vibrio cholerae O1 Cholera Toxin

Microbiology ◽  
1989 ◽  
Vol 135 (5) ◽  
pp. 1195-1200 ◽  
Author(s):  
M. L. Tamplin ◽  
M. K. Ahmed ◽  
R. Jalali ◽  
R. R. Colwell
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
B Subunit ◽  
Vibrio Cholerae O1 ◽  
El Tor

scholarly journals Back to the Future: Studying Cholera Pathogenesis Using Infant Rabbits

mBio ◽  
2010 ◽  
Vol 1 (1) ◽  
Author(s):  
Jennifer M. Ritchie ◽  
Haopeng Rui ◽  
Roderick T. Bronson ◽  
Matthew K. Waldor
Keyword(s):  
Animal Model ◽  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Close Association ◽  
Disease Model ◽  
Rabbit Model ◽  
Secretory Diarrhea ◽  
Watery Diarrhea ◽  
Content Type

ABSTRACTCholera is a severe diarrheal disease, caused byVibrio cholerae, for which there has been no reproducible, nonsurgical animal model. Here, we report that orogastric inoculation ofV. choleraeinto 3-day-old rabbits pretreated with cimetidine led to lethal, watery diarrhea in virtually all rabbits. The appearance and chemical composition of the rabbit diarrheal fluid were comparable to those of the “rice-water stool” produced by cholera patients. As in humans,V. choleraemutants that do not produce cholera toxin (CT) and toxin-coregulated pilus (TCP) did not induce cholera-like disease in rabbits. CT induced extensive exocytosis of mucin from intestinal goblet cells, and wild-typeV. choleraewas predominantly found in close association with mucin. Large aggregates of mucin-embeddedV. choleraewere observed, both attached to the epithelium and floating within the diarrheal fluid. These findings suggest that CT-dependent mucin secretion significantly influencesV. cholerae’s association with the host intestine and its exit from the intestinal tract. Our model should facilitate identification and analyses of factors that may governV. choleraeinfection, survival, and transmission, such as mucin. In addition, our results using nontoxigenicV. choleraesuggest that infant rabbits will be useful for study of the reactogenicity of live attenuated-V. choleraevaccines.IMPORTANCECholera remains a significant threat to populations in developing nations. Currently, there is no reproducible, nonsurgical animal model of cholera, the secretory diarrheal disease caused byVibrio cholerae. We found that oral infection of infant rabbits withV. choleraeled to lethal, watery diarrhea in most rabbits. Using this disease model, we discovered a new role for cholera toxin (CT) during infection. This toxin not only caused secretory diarrhea but also profoundly influenced howV. choleraeassociates with the intestine and how the pathogen exits from the host. Rabbits inoculated withV. choleraethat does not produce CT developed mild diarrhea, suggesting that this model may prove useful for generating improved live attenuated-V. choleraevaccine candidates. Overall, our findings suggest that the infant rabbit model will enable pursuit of several new avenues for research on cholera pathogenesis, as well as serve as a vehicle for testing new therapeutics.

scholarly journals Whole-Genome Sequencing of Vibrio cholerae O1 El Tor Strains Isolated in Ukraine (2011) and Russia (2014)

2017 ◽  
Vol 5 (8) ◽  
Author(s):  
Nina I. Smirnova ◽  
Yaroslav M. Krasnov ◽  
Elena Y. Agafonova ◽  
Elena Y. Shchelkanova ◽  
Zhanna V. Alkhova ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Genome Sequencing ◽  
Genetic Similarity ◽  
Whole Genome Sequence ◽  
Whole Genome ◽  
Content Type ◽  
Vibrio Cholerae O1 ◽  
El Tor ◽  
Highly Virulent ◽  
High Genetic Similarity

ABSTRACT Here, we present the draft whole-genome sequence of Vibrio cholerae O1 El Tor strains 76 and M3265/80, isolated in Mariupol, Ukraine, and Moscow, Russia. The presence of various mutations detected in virulence-associated mobile elements indicates high genetic similarity of the strains reported here with new highly virulent variants of the cholera agent V. cholerae.

scholarly journals Cholera Toxin Production by the El Tor Variant of Vibrio cholerae O1 Compared to Prototype El Tor and Classical Biotypes

2010 ◽  
Vol 48 (11) ◽  
pp. 4283-4286 ◽  
Author(s):  
J. Ghosh-Banerjee ◽  
M. Senoh ◽  
T. Takahashi ◽  
T. Hamabata ◽  
S. Barman ◽  
...  
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Toxin Production ◽  
Vibrio Cholerae O1 ◽  
El Tor

Classical RS1 and environmental RS1 elements in Vibrio cholerae O1 El Tor strains harbouring a tandem repeat of CTX prophage: revisiting Mozambique in 2005

2010 ◽  
Vol 59 (3) ◽  
pp. 302-308 ◽  
Author(s):  
Seon Young Choi ◽  
Je Hee Lee ◽  
Eun Jin Kim ◽  
Hye Ri Lee ◽  
Yoon-Seong Jeon ◽  
...  
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Tandem Repeat ◽  
Small Chromosome ◽  
Classical Type ◽  
Large Chromosome ◽  
New Type ◽  
Vibrio Cholerae O1 ◽  
Ctx Prophage ◽  
El Tor

Currently, Vibrio cholerae O1 serogroup biotype El Tor strains producing classical type cholera toxin (altered strains or El Tor variants) are prevalent in Asia and in Mozambique. Mozambican strains collected in 2004 contained a tandem repeat of CTX prophage on the small chromosome and each CTX prophage harboured the classical rstR and classical ctxB. We found that the majority of the strains collected in 2005 in Mozambique contained extra elements on the large chromosome in addition to the tandem repeat of CTX prophage on the small chromosome. New type RS1 elements RS1cla and RS1env, and a CTXenv with rstR env and the classical ctxB were identified on the large chromosome of the Mozambican isolates collected in 2005.

scholarly journals Serotype has a significant impact on the virulence of 7th pandemic Vibrio cholerae O1

2020 ◽  
Author(s):  
Stefan L Nordqvist ◽  
Kaisa Thorell ◽  
Frida Nilsson ◽  
Madeleine Löfstrand ◽  
Arvid Hagelberg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Vibrio Cholerae ◽  
Virulence Genes ◽  
Diarrheal Disease ◽  
Selective Pressure ◽  
Infection Model ◽  
Infant Mouse ◽  
Mouse Infection Model ◽  
Vibrio Cholerae O1 ◽  
El Tor

AbstractOf over 200 different identified Vibrio cholerae serogroups only the O1 serogroup is consistently associated with endemic and epidemic cholera disease. The O1 serogroup has two serologically distinguishable variants, the Ogawa and Inaba serotypes, which differ only by a methyl group present on the terminal sugar of the Ogawa O-antigen but absent from Inaba strains. This methylation is catalyzed by a methyltransferase encoded by the wbeT gene, which in Inaba strains is disrupted by mutation. It is currently thought that there is little difference between the two serotypes. However, here we show, using isogenic pairs of O1 El Tor V. cholerae, that Inaba strains show significantly different patterns of gene expression and are significantly less able than the corresponding Ogawa strains to cause cholera in an infant mouse infection model. Our results suggest that changes in gene expression resulting from the loss of the wbeT gene lead to reduced virulence and possibly also reduced survival fitness outside the human host.Author SummaryThe bacterium Vibrio cholerae causes the pandemic diarrheal disease cholera. Despite many identified serotypes of V. cholerae only one, O1, causes pandemic cholera. The O1 serotype of pandemic V. cholerae has two distinguishable variants (called Ogawa and Inaba) long considered to be clinically and epidemiologically equivalent. Cholera outbreaks consist only of one the two variants at any time. In general, Ogawa strains cause the majority of outbreaks with relatively short-lived Inaba outbreaks occurring sporadically. We have suggested earlier that Inaba outbreaks occur during periods of environmental selective pressure against the Ogawa serotype. We demonstrate here that the two variants are not clinically equivalent. The Ogawa serotype is better able to respond to infection in an animal model by up regulating the expression of virulence genes essential for disease development. We suggest that this phenomenon is the result of wider ranging differences in gene expression resulting from the mutation that converts Ogawa into Inaba strains, and may help to explain the dominance of the Ogawa serotype in nature.

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