Heterogeneity in the organization of the CTX genetic element in strains ofVibrio choleraeO139 Bengal isolated from Calcutta, India and Dhaka, Bangladesh and its possible link to the dissimilar incidence of O139 cholera in the two locales

Basu, Arnab; Mukhopadhyay, Asish K.; Sharma, Charu; Jyot, Jeevan; Gupta, Naveen; Ghosh, Amit; Sk, Bhattacharya; Takeda, Yoshifumi; Faruque, A. S. G.; Albert, M. John; Nair, G. Balakrish

doi:10.1006/mpat.1997.0186

Cited by 34 publications

(36 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For example, O1 classical strains have two copies of the CTX, one located on each of the two chromosomes. Also, some El Tor strains contain a single copy, while many others have two or more copies arranged in tandem on chromosome I (5,12,15,31,32,34). V. cholerae O139 strains are similar to O1 El Tor strains in that they have two copies of the CTX arranged in tandem on chromosome I (5, 56).…”

Section: Discussionmentioning

confidence: 99%

Evidence for the Emergence of Non-O1 and Non-O139 Vibrio cholerae Strains with Pathogenic Potential by Exchange of O-Antigen Biosynthesis Regions

Shimada

Morris

et al. 2002

Infect Immun

View full text Add to dashboard Cite

The novel epidemic strain Vibrio cholerae O139 Bengal originated from a seventh-pandemic O1 El Tor strain by antigenic shift resulting from homologous recombination-mediated exchange of O-antigen biosynthesis (wb*) clusters. Conservation of the genetic organization of wb* regions seen in other serogroups raised the possibility of the existence of pathogenic non-O1 and non-O139 V. cholerae strains that emerged by similar events. To test this hypothesis, 300 V. cholerae isolates of non-O1 and non-O139 serogroups were screened for the presence of virulence genes and an epidemic genetic background by DNA dot blotting, IS1004 fingerprinting, and restriction fragment length polymorphism (RFLP) analysis. We found four non-O1 strains (serogroups O27, O37, O53, and O65) with an O1 genetic backbone suggesting exchange of wb* clusters. DNA sequence analysis of the O37 wb* region revealed that a novel ϳ23.4-kb gene cluster had replaced all but the ϳ4.2-kb right junction of the 22-kb O1 wbe region. In sharp contrast to the backbones, the virulence regions of the four strains were quite heterogeneous; the O53 and O65 strains had the El Tor vibrio pathogenicity island (VPI) cluster, the O37 strain had the classical VPI cluster, and the O27 strain had a novel VPI cluster. Two of the four strains carried CTX; the O27 strain possessed a CTX with a recently reported immune specificity (rstR-4** allele) and a novel ctxB allele, and the O37 strain had an El Tor CTX (rstR ET allele) and novel ctxAB alleles. Although the O53 and O65 strains lacked the ctxAB genes, they carried a pre-CTX (i.e., rstR cla ). Identification of non-O1 and non-O139 serogroups with pathogenic potential in epidemic genetic backgrounds means that attention should be paid to possible future epidemics caused by these serogroups and to the need for new, rapid vaccine development strategies.

show abstract

Section: Discussionmentioning

confidence: 99%

Evidence for the Emergence of Non-O1 and Non-O139 Vibrio cholerae Strains with Pathogenic Potential by Exchange of O-Antigen Biosynthesis Regions

Shimada

Morris

et al. 2002

Infect Immun

View full text Add to dashboard Cite

show abstract

“…The 24 environmental isolates of V. cholerae studied here were obtained from water samples from Calcutta, India, by enrichment culture (8 of 122 tested) and PCR-based screening for tcpA (classical or El Tor) or ctx genes and O-antigen typing, as described previously (8) (Table 1). Three reference epidemic strains of V. cholerae were also used: O139 (SG24); O1 Ogawa, El Tor biotype (VC20); and O1, Ogawa, classical biotype (O395) (2).…”

Section: Methodsmentioning

confidence: 99%

Characterization of VPI Pathogenicity Island and CTXφ Prophage in Environmental Strains of Vibrio cholerae

et al. 2001

Self Cite

View full text Add to dashboard Cite

Environmental isolates of Vibrio cholerae of eight randomly amplified polymorphic DNA (RAPD) fingerprint types from Calcutta, India, that were unusual in containing toxin-coregulated pilus or cholera toxin genes but not O1 or O139 antigens of epidemic strains were studied by PCR and sequencing to gain insights into V. cholerae evolution. We found that each isolate contained a variant form of the VPI pathogenicity island. Distinguishing features included (i) four new alleles of tcpF (which encodes secreted virulence protein; its exact function is unknown), 20 to 70% divergent (at the protein level) from each other and canonical tcpF; (ii) a new allele of toxT (virulence regulatory gene), 36% divergent (at the protein level) in its 5 half and nearly identical in its 3 half to canonical toxT; (iii) a new tcpA (pilin) gene; and (iv) four variant forms of a regulatory sequence upstream of toxT. Also found were transpositions of an IS903-related element and function-unknown genes to sites in VPI. Cholera toxin (ctx) genes were found in isolates of two RAPD types, in each case embedded in CTX-like prophages. Fragments that are inferred to contain only putative repressor, replication, and integration genes were present in two other RAPD types. New possible prophage repressor and replication genes were also identified. Our results show marked genetic diversity in the virulence-associated gene clusters found in some nonepidemic V. cholerae strains, suggest that some of these genes contribute to fitness in nature, and emphasize the potential importance of interstrain gene exchange in the evolution of this species.Vibrio cholerae is a genetically diverse species that lives in warm-water environments, often associated with plankton and other aquatic organisms (9, 15, 31). Strains of just two of the approximately 200 currently known O-antigen serogroups (50; T. Shimada, personal communication), O1 and O139, cause epidemic cholera-the acute, devastating diarrheal disease that afflicts many thousands of people annually, especially in developing countries. Although certain other serogroups cause sporadic diarrheal disease (30, 37), most V. cholerae organisms probably do not infect humans. Epidemic strains are also distinguished from most others by their production of cholera toxin and a toxin-coregulated pilus (TCP) (15,21).Epidemic strains of V. cholerae have a complex natural history in areas of cholera endemicity, involving rapid transmission to humans via contaminated food and water during each year's cholera season and persistence or proliferation in aquatic organisms or abiotic niches at other times. Several recent major changes in patterns of epidemic cholera may stem in large part from a combination of human factors and environmental fluctuation that could affect the distribution of aquatic host species. The bacterial changes include (i) the replacement of classical biotype O1 strains beginning in 1961 by strains of the new El Tor O1 biotype (15), (ii) the reemergence of classical biotype strains in parts of Bangladesh i...

show abstract

“…Second, strains differ by the number of phage genomes and RS1s that they contain and in the relative arrangements of these elements. Numerous patterns have been detected in O1 El Tor strains as well as in O139 strains (4,13,21). In contrast, the majority of classical strains have been thought, based on restriction mapping, to share a single arrangement (13).…”

mentioning

confidence: 99%

CTX Prophages in Classical Biotype Vibrio cholerae : Functional Phage Genes but Dysfunctional Phage Genomes

et al. 2000

View full text Add to dashboard Cite

CTX is a filamentous, lysogenic bacteriophage whose genome encodes cholera toxin, the primary virulence factor produced by Vibrio cholerae. CTX prophages in O1 El Tor and O139 strains of V. cholerae are found within arrays of genetically related elements integrated at a single locus within the V. cholerae large chromosome. The prophages of O1 El Tor and O139 strains generally yield infectious CTX. In contrast, O1 classical strains of V. cholerae do not produce CTX, although they produce cholera toxin and they contain CTX prophages integrated at two sites. We have identified the second site of CTX prophage integration in O1 classical strains and characterized the classical prophage arrays genetically and functionally. The genes of classical prophages encode functional forms of all of the proteins needed for production of CTX. Classical CTX prophages are present either as solitary prophages or as arrays of two truncated, fused prophages. RS1, a genetic element that is closely related to CTX and is often interspersed with CTX prophages in El Tor strains, was not detected in classical V. cholerae. Our model for CTX production predicts that the CTX prophage arrangements in classical strains will not yield extrachromosomal CTX DNA and thus will not yield virions, and our experimental results confirm this prediction. Thus, failure of O1 classical strains of V. cholerae to produce CTX is due to overall deficiencies in the structures of the arrays of classical prophages, rather than to mutations affecting individual CTX prophage genes.The severe diarrheal disease cholera results from colonization of the human small intestine by pathogenic strains of a gram-negative bacterium, Vibrio cholerae. Cholera has afflicted human populations in many parts of the world for more than a millenium (2). Widespread outbreaks have been common; in the last 200 years alone, seven cholera pandemics have occurred. Most epidemic strains of V. cholerae have been of the O1 serogroup, although in the last 8 years O139 serogroup strains of V. cholerae have also been linked to disease outbreaks (23). The O1 serogroup of V. cholerae has been divided into strains of the classical biotype, thought to have been responsible for the first six cholera pandemics, and the El Tor biotype, which has caused the ongoing seventh pandemic (2). These El Tor and classical strains have traditionally been differentiated in the laboratory with assays of hemolysis, hemagglutination, phage sensitivity, and polymyxin sensitivity and with the Voges-Proskauer reaction (23). Genetic typing of strains has also become possible in recent years. However, despite their phenotypic and genotypic differences, the symptoms of infection with strains of the two O1 biotypes are clinically indistinguishable. The clinical manifestations of cholera are almost entirely due to production of cholera toxin, a potent A-B-type exotoxin that is secreted by pathogenic V. cholerae (10).The genes that encode cholera toxin, ctxAB, reside within the genome of a filamentous, lysogenic bacteriophage k...

show abstract

Heterogeneity in the organization of the CTX genetic element in strains ofVibrio choleraeO139 Bengal isolated from Calcutta, India and Dhaka, Bangladesh and its possible link to the dissimilar incidence of O139 cholera in the two locales

Cited by 34 publications

References 27 publications

Evidence for the Emergence of Non-O1 and Non-O139 Vibrio cholerae Strains with Pathogenic Potential by Exchange of O-Antigen Biosynthesis Regions

Evidence for the Emergence of Non-O1 and Non-O139 Vibrio cholerae Strains with Pathogenic Potential by Exchange of O-Antigen Biosynthesis Regions

Characterization of VPI Pathogenicity Island and CTXφ Prophage in Environmental Strains of Vibrio cholerae

CTX Prophages in Classical Biotype Vibrio cholerae : Functional Phage Genes but Dysfunctional Phage Genomes

Contact Info

Product

Resources

About