A search for cholera toxin (CT), toxin coregulated pilus (TCP), the regulatory element ToxR and other virulence factors in non-O1/non-O139Vibrio cholerae

Ghosh, Chandradipa; Nandy, Ranjan K.; Dasgupta, Saumya; Nair, G. Balakrish; Hall, Ross H.; Ghose, A.M.

doi:10.1006/mpat.1996.0105

Cited by 66 publications

(78 citation statements)

References 43 publications

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“…The plasmids were transformed into E. coli JM109 competent cells, and the sequence of the cloned genes in the vector pMD 18-T was confirmed by DNA sequencing (Invitrogen Biotech, Shanghai, China). Previous studies have shown the distribution of different virulence genes among V. cholerae, V. mimicus, V. alginolyticus and V. parahaemolyticus (Ghosh et al, 1997;Sechi et al, 2000;Shi et al, 1998;Shinoda and Nakagawa, 2004;Xie et al, 2005). Our results indicate that the virulence genes such as toxS, flaB and flaC are widely distributed among different vibrios, whereas zot and tcpA only exit in a few vibrios.…”

supporting

confidence: 52%

Distribution of five vibrio virulence-related genes among Vibrio harveyi isolates

Bai

Pang

et al. 2008

J. Gen. Appl. Microbiol.

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Vibrio are widely distributed in aquatic environments (Thompson et al., 2006) and are commonly associated with marine living species and include many important pathogens for farmed animals and humans who consume contaminated seafood or polluted drinking water. Pathogenic mechanisms are only clearly understood for V. cholerae and V. parahaemolyticus, but not for the majority of other vibrios (Faruque et al., 1998;Nishibuchi and Kaper, 1995;Thompson et al., 2006). Many virulence genes have been elucidated, including the tdh gene (coding thermostable direct haemolysin) in V. parahemolyticus, ctxAB genes (coding the potent cholera toxin) in V. cholera and others (Faruque et al., 1998;Nishibuchi and Kaper, 1995).Zot (zonula occludens toxin) was first discovered in V. cholerae, and has the ability to increase the permeability of the small intestinal mucosa by affecting the structure of the intercellular tight junction, or zonula occludens (Fasano et al., 1991). The toxS gene was also first discovered in V. cholerae, and lies downstream from the toxR gene, which encodes the transcriptional activator for the cholera toxin (ctx ) operon in V. cholerae (Dirita and Mekalanos, 1991;Miller et al., 1989). toxS acts in conjunction with toxR to activate expression of the ctx operon (Miller et al., 1989). tcpA is an important virulence gene of V. cholerae, encoding the major subunit of the toxin-coregulation pilus (TCP), which exerts important roles in infection as the colonization factor (Faast et al., 1989). The importance of the flagellum in virulence has been demonstrated for several species, as either a motility organelle or an organelle that carries an adhesive component (Lee et al., 2006;Milton et al., 1996). V. cholerae contains five different structural genes of the flagellum: flgI, flgJ, flgM, flgL and flaA, and these genes encode the Pand L-ring proteins, the hook-associated proteins 1,3 and the flagellin core protein of the flagellum, respectively (Das et al., 1998).V. harveyi is a serious pathogen of marine animals . However, the virulence factors of V. harveyi are not completely understood. Previous studies have shown that the virulence factors, such as VHH haemolysin, protease, phospholipse, lipopolysaccharide and bacteriocin-like substances may contribute to the virulence of this species Zhang et al., 2001). It has been proposed that the virulence genes could be horizontally transferred among Vibrio spp. (Waldor and Mekalanos, 1996). Previously, we found that the vhh/tlh haemolysin gene and toxR gene exit in all V. harveyi strains detected (Pang et al

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confidence: 52%

Distribution of five vibrio virulence-related genes among Vibrio harveyi isolates

Bai

Pang

et al. 2008

J. Gen. Appl. Microbiol.

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“…Strains that can trigger epidemics may acquire virulence genes successively (9,10,20,45) (12,24,28,42,43,46). Variable gene sequences of pIII CTX have also been documented (9,11).…”

Section: Discussionmentioning

confidence: 99%

“…In other words, perhaps these strains (or similar strains) have the potential to become new dominant clones in future epidemics through the acquisition of CTX⌽ with the corresponding pIII CTX allele. Obvious divergence in virulence-related genes such as tcpA (12,21,24,28,42,43,46), the gene for pIII CTX (9,11), and rstR (9,14,15) in CTX⌽ has been found in different strains. Similarly, sequence variance in the ompU, pilA, and EPS cluster was also observed in nontoxigenic O1 V. cholerae in our study.…”

Section: Discussionmentioning

confidence: 99%

Genetic Diversity of Toxigenic and Nontoxigenic Vibrio cholerae Serogroups O1 and O139 Revealed by Array-Based Comparative Genomic Hybridization

et al. 2007

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Toxigenic serogroups O1 and O139 of Vibrio cholerae may cause cholera epidemics or pandemics. Nontoxigenic strains within these serogroups also exist in the environment, and also some may cause sporadic cases of disease. Herein, we investigate the genomic diversity among toxigenic and nontoxigenic O1 and O139 strains by comparative genomic microarray hybridization with the genome of El Tor strain N16961 as a base. Conservation of the toxigenic O1 El Tor and O139 strains is found as previously reported, whereas accumulation of genome changes was documented in toxigenic El Tor strains isolated within the 40 years of the seventh pandemic. High phylogenetic diversity in nontoxigenic O1 and O139 strains is observed, and most of the genes absent from nontoxigenic strains are clustered together in the N16961 genome. By comparing these toxigenic and nontoxigenic strains, we observed that the small chromosome of V. cholerae is quite conservative and stable, outside of the superintegron region. In contrast to the general stability of the genome, the superintegron demonstrates pronounced divergence among toxigenic and nontoxigenic strains. Additionally, sequence variation in virulence-related genes is found in nontoxigenic El Tor strains, and we speculate that these intermediate strains may have pathogenic potential should they acquire CTX prophage alleles and other gene clusters. This genome-wide comparison of toxigenic and nontoxigenic V. cholerae strains may promote understanding of clonal differentiation of V. cholerae and contribute to an understanding of the origins and clonal selection of epidemic strains.

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“…The ctxAB genes, which encode CT, are integral components of a novel filamentous phage CTX (64), and the TCP biosynthesis genes are encoded on the Vibrio pathogenicity island (hereafter designated VPI-1) (35). A number of studies have found that the two main virulence factors, CT and TCP, are predominately associated with V. cholerae O1 and O139 serogroup strains and are only occasionally found in nonepidemic isolates (5,7,8,10,13,25,40,47,49,50,55).…”

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confidence: 99%

Evolutionary Genetic Analysis of the Emergence of Epidemic Vibrio cholerae Isolates on the Basis of Comparative Nucleotide Sequence Analysis and Multilocus Virulence Gene Profiles

et al. 2004

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Vibrio cholerae, the causative agent of cholera, is a natural inhabitant of the aquatic ecosystem. We examined a unique collection of V. cholerae clinical and environmental isolates of widespread geographic distribution recovered over a 60-year period to determine their evolutionary genetic relationships based on analysis of two housekeeping genes, malate dehydrogenase (mdh) and a chaperonin (groEL). In addition, the phylogenetic distribution of 12 regions associated with virulence was determined. Comparative sequence analysis of mdh revealed that all V. cholerae O1 and O139 serogroup isolates belonged to the same clonal lineage. Single-strand conformational polymorphism (SSCP) analysis of these O1 and O139 strains at groEL confirmed the presence of an epidemic clonal complex. Of the 12 virulence regions examined, only three regions, Vibrio seventh pandemic island 1 (VSP-I), VSP-II, and RS1, were absent from all classical V. cholerae isolates. Most V. cholerae El Tor biotype and O139 serogroup isolates examined encoded all 12 virulence regions assayed. Outside of V. cholerae O1/O139 serogroup isolates, only one strain, VO7, contained VSP-I. Two V. cholerae El Tor isolates, GP155 and 2164-78, lacked both VSP-I and VSP-II, and one El Tor isolate, GP43, lacked VSP-II. Five non-O1/non-O139 serogroup isolates had an mdh sequence identical to that of the epidemic O1 and O139 strains. These isolates, similar to classical strains, lack both VSP-I and VSP-II. Four of the 12 virulence regions examined were found to be present in all isolates: hlyA, pilE, MSHA and RTX. Among non-O1/non-O139 isolates, however, the occurrence of the additional eight regions was considerably lower. The evolutionary relationships and multilocus virulence gene profiles of V. cholerae natural isolates indicate that consecutive pandemic strains arose from a common O1 serogroup progenitor through the successive acquisition of new virulence regions.

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A search for cholera toxin (CT), toxin coregulated pilus (TCP), the regulatory element ToxR and other virulence factors in non-O1/non-O139Vibrio cholerae

Cited by 66 publications

References 43 publications

Distribution of five vibrio virulence-related genes among Vibrio harveyi isolates

Distribution of five vibrio virulence-related genes among Vibrio harveyi isolates

Genetic Diversity of Toxigenic and Nontoxigenic Vibrio cholerae Serogroups O1 and O139 Revealed by Array-Based Comparative Genomic Hybridization

Evolutionary Genetic Analysis of the Emergence of Epidemic Vibrio cholerae Isolates on the Basis of Comparative Nucleotide Sequence Analysis and Multilocus Virulence Gene Profiles

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