scholarly journals Examination of Diverse Toxin-Coregulated Pilus-Positive Vibrio cholerae Strains Fails To Demonstrate Evidence for Vibrio Pathogenicity Island Phage

2003 ◽  
Vol 71 (6) ◽  
pp. 2993-2999 ◽  
Author(s):  
Shah M. Faruque ◽  
Jun Zhu ◽  
Asadulghani ◽  
M. Kamruzzaman ◽  
John J. Mekalanos
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Genetic Variants ◽  
Horizontal Transfer ◽  
Pathogenicity Island ◽  
Culture Conditions ◽  
Filamentous Phage ◽  
Colonization Factor ◽  
Toxin Coregulated Pilus ◽  
El Tor

ABSTRACT The major virulence factors of toxigenic Vibrio cholerae are cholera toxin, which is encoded by a lysogenic filamentous bacteriophage (CTXΦ), and toxin-coregulated pilus (TCP), an essential colonization factor that is also the receptor for CTXΦ. The genes involved in the biosynthesis of TCP reside in a pathogenicity island, which has been reported to correspond to the genome of another filamentous phage (designated VPIΦ) and to encode functions necessary for the production of infectious VPIΦ particles. We examined 46 V. cholerae strains having diverse origins and carrying different genetic variants of the TCP island for the production of the VPIΦ and CTXΦ in different culture conditions, including induction of prophages with mitomycin C and UV irradiation. Although 9 of 10 V. cholerae O139 strains and 12 of 15 toxigenic El Tor strains tested produced extracellular CTXΦ, none of the 46 TCP-positive strains produced detectable VPIΦ in repeated assays, which detected as few as 10 particles of a control CTX phage per ml. These results contradict the previous report regarding VPIΦ-mediated horizontal transfer of the TCP genes and suggest that the TCP island is unable to support the production of phage particles. Further studies are necessary to understand the mechanism of horizontal transfer of the TCP island.

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 The Cyclic Dipeptide Cyclo(Phe-Pro) Inhibits Cholera Toxin and Toxin-Coregulated Pilus Production in O1 El Tor Vibrio cholerae

2010 ◽  
Vol 192 (14) ◽  
pp. 3829-3832 ◽  
Author(s):  
Xiaowen R. Bina ◽  
James E. Bina
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Virulence Gene ◽  
Cyclic Dipeptide ◽  
Present Evidence ◽  
Toxin Coregulated Pilus ◽  
El Tor ◽  
Virulence Regulator

ABSTRACT Cyclo(Phe-Pro) is a cyclic dipeptide produced by multiple Vibrio species. In this work, we present evidence that cyclo(Phe-Pro) inhibits the production of the virulence factors cholera toxin (CT) and toxin-coregulated pilus (TCP) in O1 El Tor Vibrio cholerae strain N16961 during growth under virulence gene-inducing conditions. The cyclo(Phe-Pro) inhibition of CT and TCP production correlated with reduced transcription of the virulence regulator tcpPH and was alleviated by overexpression of tcpPH.

scholarly journals Comparative Genomic Analyses of the Vibrio Pathogenicity Island and Cholera Toxin Prophage Regions in Nonepidemic Serogroup Strains of Vibrio cholerae

2003 ◽  
Vol 69 (3) ◽  
pp. 1728-1738 ◽  
Author(s):  
Manrong Li ◽  
Mamuka Kotetishvili ◽  
Yuansha Chen ◽  
Shanmuga Sozhamannan
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Fragment Length Polymorphism ◽  
Pathogenicity Island ◽  
Filamentous Phage ◽  
Comparative Genomic ◽  
Genomic Analyses ◽  
Ctxφ Prophage ◽  
Horizontal Acquisition ◽  
Restriction Fragment Length

ABSTRACT Two major virulence factors are associated with epidemic strains (O1 and O139 serogroups) of Vibrio cholerae: cholera toxin encoded by the ctxAB genes and toxin-coregulated pilus encoded by the tcpA gene. The ctx genes reside in the genome of a filamentous phage (CTXφ), and the tcpA gene resides in a vibrio pathogenicity island (VPI) which has also been proposed to be a filamentous phage designated VPIφ. In order to determine the prevalence of horizontal transfer of VPI and CTXφ among nonepidemic (non-O1 and non-O139 serogroups) V. cholerae, 300 strains of both clinical and environmental origin were screened for the presence of tcpA and ctxAB. In this paper, we present the comparative genetic analyses of 11 nonepidemic serogroup strains which carry the VPI cluster. Seven of the 11 VPI+ strains have also acquired the CTXφ. Multilocus sequence typing and restriction fragment length polymorphism analyses of the VPI and CTXφ prophage regions revealed that the non-O1 and non-O139 strains were genetically diverse and clustered in lineages distinct from that of the epidemic strains. The left end of the VPI in the non-O1 and non-O139 strains exhibited extensive DNA rearrangements. In addition, several CTXφ prophage types characterized by novel repressor (rstR) and ctxAB genes and VPIs with novel tcpA genes were found in these strains. These data suggest that the potentially pathogenic, nonepidemic, non-O1 and non-O139 strains identified in our study most likely evolved by sequential horizontal acquisition of the VPI and CTXφ independently rather than by exchange of O-antigen biosynthesis regions in an existing epidemic strain.

scholarly journals A Vibrio cholerae LysR Homolog, AphB, Cooperates with AphA at the tcpPH Promoter To Activate Expression of the ToxR Virulence Cascade

1999 ◽  
Vol 181 (14) ◽  
pp. 4250-4256 ◽  
Author(s):  
Gabriela Kovacikova ◽  
Karen Skorupski
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Genes ◽  
Virulence Gene ◽  
Growth Conditions ◽  
Culture Conditions ◽  
Virulence Gene Expression ◽  
Environmental Stimuli ◽  
High Level ◽  
El Tor

ABSTRACT We describe here a new member of the LysR family of transcriptional regulators, AphB, which is required for activation of the Vibrio cholerae ToxR virulence cascade. AphB activates the transcription of the tcpPH operon in response to environmental stimuli, and this process requires cooperation with a second protein, AphA. The expression of neither aphA or aphB is strongly regulated by environmental stimuli, raising the possibility that the activities of the proteins themselves may be influenced under various conditions. Strains of the El Tor biotype of V. choleraetypically exhibit lower expression of ToxR-regulated virulence genes in vitro than classical strains and require specialized culture conditions (AKI medium) to induce high-level expression. We show here that expression of aphB from the tac promoter in El Tor biotype strains dramatically increases virulence gene expression to levels similar to those observed in classical strains under all growth conditions examined. These results suggest that AphB plays a role in the differential regulation of virulence genes between the two disease-causing biotypes.

scholarly journals TcpF Is a Soluble Colonization Factor and Protective Antigen Secreted by El Tor and Classical O1 and O139 Vibrio cholerae Serogroups

2005 ◽  
Vol 73 (8) ◽  
pp. 4461-4470 ◽  
Author(s):  
Thomas J. Kirn ◽  
Ronald K. Taylor
Keyword(s):  
Vibrio Cholerae ◽  
Protective Antigen ◽  
Secretion System ◽  
Cholera Vaccine ◽  
Infant Mouse ◽  
Bacterial Interactions ◽  
Secretion Pathway ◽  
Extracellular Secretion ◽  
Colonization Factor ◽  
El Tor

ABSTRACT Vibrio cholerae causes diarrhea by colonizing the human small bowel and intoxicating epithelial cells. Colonization is a required step in pathogenesis, and strains defective for colonization are significantly attenuated. The best-characterized V. cholerae colonization factor is the toxin-coregulated pilus (TCP). It has been demonstrated that TCP is required for V. cholerae colonization in both humans and mice. TCP enhances bacterial interactions that allow microcolony formation and thereby promotes survival in the intestine. We have recently discovered that the TCP biogenesis apparatus also serves as a secretion system, mediating the terminal step in the extracellular secretion pathway of TcpF. TcpF was identified in classical isolates of V. cholerae O1 as a soluble factor essential for colonization in the infant mouse cholera model. In the present study, we expanded our analysis of TcpF to include the O1 El Tor and O139 serogroups and investigated how TCP and TcpF act together to mediate colonization. Additionally, we demonstrated that antibodies generated against TcpF are protective against experimental V. cholerae infection in the infant mouse cholera model. This observation, coupled with the fact that TcpF is a potent mediator of colonization, suggests that TcpF should be considered as a component of a polyvalent cholera vaccine formulation.

scholarly journals RS1 Element of Vibrio cholerae Can Propagate Horizontally as a Filamentous Phage Exploiting the Morphogenesis Genes of CTXΦ

2002 ◽  
Vol 70 (1) ◽  
pp. 163-170 ◽  
Author(s):  
Shah M. Faruque ◽  
Asadulghani ◽  
M. Kamruzzaman ◽  
Ranjan K. Nandi ◽  
A. N. Ghosh ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Kanamycin Resistance ◽  
Open Reading Frames ◽  
Filamentous Phage ◽  
Pcr Analysis ◽  
Recombination System ◽  
Genes Encoding ◽  
Ctx Prophage ◽  
A Site ◽  
El Tor

ABSTRACT In toxigenic Vibrio cholerae, cholera toxin is encoded by the CTX prophage, which consists of a core region carrying ctxAB genes and genes required for CTXΦ morphogenesis, and an RS2 region encoding regulation, replication, and integration functions. Integrated CTXΦ is often flanked by another genetic element known as RS1 which carries all open reading frames (ORFs) found in RS2 and an additional ORF designated rstC. We identified a single-stranded circularized form of the RS1 element, in addition to the CTXΦ genome, in nucleic acids extracted from phage preparations of 32 out of 83 (38.5%) RS1-positive toxigenic V. cholerae strains analyzed. Subsequently, the corresponding double-stranded replicative form (RF) of the RS1 element was isolated from a representative strain and marked with a kanamycin resistance (Kmr) marker in an intergenic site to construct pRS1-Km. Restriction and PCR analysis of pRS1-Km and sequencing of a 300-bp region confirmed that this RF DNA was the excised RS1 element which formed a novel junction between ig1 and rstC. Introduction of pRS1-Km into a V. cholerae O1 classical biotype strain, O395, led to the production of extracellular Kmr transducing particles, which carried a single-stranded form of pRS1-Km, thus resembling the genome of a filamentous phage (RS1-KmΦ). Analysis of V. cholerae strains for susceptibility to RS1-KmΦ showed that classical biotype strains were more susceptible to the phage compared to El Tor and O139 strains. Nontoxigenic (CTX−) O1 and O139 strains which carried genes encoding the CTXΦ receptor toxin-coregulated pilus (TCP) were also more susceptible (>1,000-fold) to the phage compared to toxigenic El Tor or O139 strains. Like CTXΦ, the RS1Φ genome also integrated into the host chromosomes by using the attRS sequence. However, only transductants of RS1-KmΦ which also harbored the CTXΦ genome produced a detectable level of extracellular RS1-KmΦ. This suggested that the core genes of CTXΦ are also required for the morphogenesis of RS1Φ. The results of this study showed for the first time that RS1 element, which encodes a site-specific recombination system in V. cholerae, can propagate horizontally as a filamentous phage, exploiting the morphogenesis genes of CTXΦ.

scholarly journals Comparison of Vibrio choleraePathogenicity Islands in Sixth and Seventh Pandemic Strains

2001 ◽  
Vol 69 (3) ◽  
pp. 1947-1952 ◽  
Author(s):  
David K. R. Karaolis ◽  
Ruiting Lan ◽  
James B. Kaper ◽  
Peter R. Reeves
Keyword(s):  
Amino Acid ◽  
Vibrio Cholerae ◽  
Virulence Factor ◽  
Virulence Genes ◽  
Preliminary Evidence ◽  
Colonization Factor ◽  
Type Iv ◽  
Factor Expression ◽  
Pandemic Strains ◽  
El Tor

ABSTRACT Epidemic Vibrio cholerae strains possess a large cluster of essential virulence genes on the chromosome called theVibrio pathogenicity island (VPI). The VPI contains thetcp gene cluster encoding the type IV pilus toxin-coregulated pilus colonization factor which can act as the cholera toxin bacteriophage (CTXΦ) receptor. The VPI also contains genes that regulate virulence factor expression. We have fully sequenced and compared the VPI of the seventh-pandemic (El Tor biotype) strain N16961 and the sixth-pandemic (classical biotype) strain 395 and found that the N16961 VPI is 41,272 bp and encodes 29 predicted proteins, whereas the 395 VPI is 41,290 bp. In addition to various nucleotide and amino acid polymorphisms, there were several proteins whose predicted size differed greatly between the strains as a result of frameshift mutations. We hypothesize that these VPI sequence differences provide preliminary evidence to help explain the differences in virulence factor expression between epidemic strains (i.e., the biotypes) of V. cholerae.

scholarly journals Expression of virulence factors by classical and El Tor Vibrio cholerae in vivo and in vitro

1990 ◽  
Vol 7 (2-3) ◽  
pp. 221-228 ◽  
Author(s):  
Gunhild Jonson ◽  
Ann-Man Svennerholm ◽  
Jan Holmgren
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Factors ◽  
El Tor
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