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.

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 Differential Transcription of the tcpPHOperon Confers Biotype-Specific Control of the Vibrio cholerae ToxR Virulence Regulon

1999 ◽  
Vol 67 (10) ◽  
pp. 5117-5123 ◽  
Author(s):  
Yvette M. Murley ◽  
Patricia A. Carroll ◽  
Karen Skorupski ◽  
Ronald K. Taylor ◽  
Stephen B. Calderwood
Keyword(s):  
Gene Expression ◽  
Vibrio Cholerae ◽  
Virulence Genes ◽  
Virulence Gene ◽  
Environmental Signals ◽  
Virulence Gene Expression ◽  
Response To Temperature ◽  
El Tor ◽  
Differential Transcription

ABSTRACT Epidemic strains of Vibrio cholerae O1 are divided into two biotypes, classical and El Tor. In both biotypes, regulation of virulence gene expression depends on a cascade in which ToxR activates expression of ToxT, and ToxT activates expression of cholera toxin and other virulence genes. In the classical biotype, maximal expression of this ToxR regulon in vitro occurs at 30°C at pH 6.5 (ToxR-inducing conditions), whereas in the El Tor biotype, production of these virulence genes only occurs under very limited conditions and not in response to temperature and pH; this difference between biotypes is mediated at the level of toxT transcription. In the classical biotype, two other proteins, TcpP and TcpH, are needed for maximal toxT transcription. Transcription oftcpPH in the classical biotype is regulated by pH and temperature independently of ToxR or ToxT, suggesting that TcpP and TcpH couple environmental signals to transcription of toxT. In this study, we show a near absence of tcpPH message in the El Tor biotype under ToxR-inducing conditions of temperature and pH. However, once expressed, El Tor TcpP and TcpH appear to be as effective as classical TcpP and TcpH in activating toxTtranscription. These results suggest that differences in regulation of virulence gene expression between the biotypes of V. cholerae primarily result from differences in expression oftcpPH message in response to environmental signals. We present an updated model for control of the ToxR virulence regulon inV. cholerae.

scholarly journals Transcutaneous Immunization with Toxin-Coregulated Pilin A Induces Protective Immunity against Vibrio cholerae O1 El Tor Challenge in Mice

2006 ◽  
Vol 74 (10) ◽  
pp. 5834-5839 ◽  
Author(s):  
Julianne E. Rollenhagen ◽  
Anuj Kalsy ◽  
Francisca Cerda ◽  
Manohar John ◽  
Jason B. Harris ◽  
...  
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Lethal Dose ◽  
Infant Mouse ◽  
Type Iv ◽  
Transcutaneous Immunization ◽  
Structural Subunit ◽  
Vibrio Cholerae O1 ◽  
The Mean ◽  
El Tor

ABSTRACT Toxin-coregulated pilin A (TcpA) is the main structural subunit of a type IV bundle-forming pilus of Vibrio cholerae, the cause of cholera. Toxin-coregulated pilus is involved in formation of microcolonies of V. cholerae at the intestinal surface, and strains of V. cholerae deficient in TcpA are attenuated and unable to colonize intestinal surfaces. Anti-TcpA immunity is common in humans recovering from cholera in Bangladesh, and immunization against TcpA is protective in murine V. cholerae models. To evaluate whether transcutaneously applied TcpA is immunogenic, we transcutaneously immunized mice with 100 μg of TcpA or TcpA with an immunoadjuvant (cholera toxin [CT], 50 μg) on days 0, 19, and 40. Mice immunized with TcpA alone did not develop anti-TcpA responses. Mice that received transcutaneously applied TcpA and CT developed prominent anti-TcpA immunoglobulin G (IgG) serum responses but minimal anti-TcpA IgA. Transcutaneous immunization with CT induced prominent IgG and IgA anti-CT serum responses. In an infant mouse model, offspring born to dams transcutaneously immunized either with TcpA and CT or with CT alone were challenged with 106 CFU (one 50% lethal dose) wild-type V. cholerae O1 El Tor strain N16961. At 48 h, mice born to females transcutaneously immunized with CT alone had 36% ± 10% (mean ± standard error of the mean) survival, while mice born to females transcutaneously immunized with TcpA and CT had 69% ± 6% survival (P < 0.001). Our results suggest that transcutaneous immunization with TcpA and an immunoadjuvant induces protective anti-TcpA immune responses. Anti-TcpA responses may contribute to an optimal cholera vaccine.

scholarly journals Transcriptional Silencing by TsrA in the Evolution of Pathogenic Vibrio cholerae Biotypes

mBio ◽  
2020 ◽  
Vol 11 (6) ◽  
Author(s):  
Florence Caro ◽  
José A. Caro ◽  
Nicole M. Place ◽  
John J. Mekalanos
Keyword(s):  
Gene Expression ◽  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Virulence Genes ◽  
Secretion System ◽  
Type Vi Secretion System ◽  
Content Type ◽  
Type Vi Secretion ◽  
Genes Encoding ◽  
El Tor

ABSTRACT Vibrio cholerae is a globally important pathogen responsible for the severe epidemic diarrheal disease called cholera. The current and ongoing seventh pandemic of cholera is caused by El Tor strains, which have completely replaced the sixth-pandemic classical strains of V. cholerae. To successfully establish infection and disseminate to new victims, V. cholerae relies on key virulence factors encoded on horizontally acquired genetic elements. The expression of these factors relies on the regulatory architecture that coordinates the timely expression of virulence determinants during host infection. Here, we apply transcriptomics and structural modeling to understand how type VI secretion system regulator A (TsrA) affects gene expression in both the classical and El Tor biotypes of V. cholerae. We find that TsrA acts as a negative regulator of V. cholerae virulence genes encoded on horizontally acquired genetic elements. The TsrA regulon comprises genes encoding cholera toxin (CT), the toxin-coregulated pilus (TCP), and the type VI secretion system (T6SS), as well as genes involved in biofilm formation. The majority of the TsrA regulon is carried on horizontally acquired AT-rich genetic islands whose loss or acquisition could be directly ascribed to the differences between the classical and El Tor strains studied. Our modeling predicts that the TsrA protein is a structural homolog of the histone-like nucleoid structuring protein (H-NS) oligomerization domain and is likely capable of forming higher-order superhelical structures, potentially with DNA. These findings describe how TsrA can integrate into the intricate V. cholerae virulence gene expression program, controlling gene expression through transcriptional silencing. IMPORTANCE Pathogenic Vibrio cholerae strains express multiple virulence factors that are encoded by bacteriophage and chromosomal islands. These include cholera toxin and the intestinal colonization pilus called the toxin-coregulated pilus, which are essential for causing severe disease in humans. However, it is presently unclear how the expression of these horizontally acquired accessory virulence genes can be efficiently integrated with preexisting transcriptional programs that are presumably fine-tuned for optimal expression in V. cholerae before its conversion to a human pathogen. Here, we report the role of a transcriptional regulator (TsrA) in silencing horizontally acquired genes encoding important virulence factors. We propose that this factor could be critical to the efficient acquisition of accessory virulence genes by silencing their expression until other signals trigger their transcriptional activation within the host.

scholarly journals VpsT Is a Transcriptional Regulator Required for Expression of vps Biosynthesis Genes and the Development of Rugose Colonial Morphology in Vibrio cholerae O1 El Tor

2004 ◽  
Vol 186 (5) ◽  
pp. 1574-1578 ◽  
Author(s):  
Catharina Casper-Lindley ◽  
Fitnat H. Yildiz
Keyword(s):  
Gene Expression ◽  
Vibrio Cholerae ◽  
Transcriptional Regulator ◽  
Response Regulators ◽  
Positive Regulator ◽  
Regulatory Systems ◽  
Two Component ◽  
Vibrio Cholerae O1 ◽  
Colonial Morphology ◽  
El Tor

ABSTRACT Vibrio cholerae switches between smooth and rugose colonial variants. The rugose variant produces more vibrio polysaccharides (VPSEl Tor) and forms well-developed biofilms. Both phenotypes depend on expression of vps biosynthesis genes. We identified a positive transcriptional regulator of vps gene expression, VpsT, which is homologous to response regulators of two-component regulatory systems. Disruption of vpsT in the rugose variant yields smooth colonies, prevents formation of mature biofilms, and decreases vps gene expression. The interaction between VpsT and VpsR, a previously identified positive regulator of vps genes, was also investigated.

Genomic Variability of Pathogenicity Islands in Nontoxigenic Strains of Vibrio cholerae O1 Biotype El Tor

2020 ◽  
Vol 56 (9) ◽  
pp. 1055-1069
Author(s):  
N. I. Smirnova ◽  
A. A. Kritsky ◽  
J. V. Alkhova ◽  
E. Yu. Agafonova ◽  
E. Yu. Shchelkanova ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Pathogenicity Islands ◽  
Genomic Variability ◽  
Vibrio Cholerae O1 ◽  
El Tor

Vibrio cholerae O1 El Tor variant and emergence of Haitian ctxB variant in the strains isolated from South India

2015 ◽  
Vol 205 (2) ◽  
pp. 195-200 ◽  
Author(s):  
Debdutta Bhattacharya ◽  
Shuchismita Dey ◽  
Gururaja Perumal Pazhani ◽  
Thandavarayan Ramamurthy ◽  
Mahantesh V. Parande ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
South India ◽  
Vibrio Cholerae O1 ◽  
El Tor

scholarly journals Isolation of Vibrio cholerae O1 strains similar to pre-seventh pandemic El Tor strains during an outbreak of gastrointestinal disease in an island resort in Fiji

2006 ◽  
Vol 55 (11) ◽  
pp. 1559-1562 ◽  
Author(s):  
G. Balakrish Nair ◽  
Ashrafus Safa ◽  
N. A. Bhuiyan ◽  
Suraia Nusrin ◽  
Denise Murphy ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Gastrointestinal Disease ◽  
Vibrio Cholerae O1 ◽  
El Tor

scholarly journals Vibrio cholerae O1 em amostras de ambientes aquáticos e de alimentos analisados no Estado de Pernambuco, Brasil

1998 ◽  
Vol 14 (3) ◽  
pp. 465-471 ◽  
Author(s):  
Waldêny Colaço ◽  
Sandoval Vieira da Silva Filho ◽  
Dália dos Prazeres Rodrigues ◽  
Ernesto Hofer
Keyword(s):  
Vibrio Cholerae ◽  
Vibrio Cholerae O1 ◽  
El Tor

No período de 1992 a 1994, foram analisadas 2.585 amostras de águas de diferentes ecossistemas, acrescidas de 91 espécimens de alimentos visando ao monitoramento de Vibrio cholerae O1 no Estado de Pernambuco. Nas 2.676 amostras foram detectadas 193 cepas de Vibrio cholerae O1 (7,21%) com predominância do sorovar Inaba (183-94,8%) sobre Ogawa (10-5,1%), todas classificadas no biotipo El Tor e sensíveis à tetraciclina. Numa parcela de setenta amostras selecionadas ao acaso, mas incluindo todas do sorovar Ogawa, foi evidenciada a produção de toxina colérica. A maior incidência do vibrião colérico em águas de rios, canais e de esgoto, representando 86% dos isolados, indicou a contaminação fecal por excretores como a causa preponderante na disseminação da bactéria nos sistemas aquáticos. Assinala-se a discreta ocorrrência de V. cholerae O1 nos alimentos processados (2,1%).

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