scholarly journals PROPERTIES OF VIBRIO CHOLERAE STRAINS ISOLATED IN ASIA AND THEIR RELATIONSHIP TO THE STRAINS CIRCULATING IN OTHER CONTINENTS DURING THE SEVENTH CHOLERA PANDEMIC

2012 ◽  
Vol 17 (1) ◽  
pp. 39-45
Author(s):  
Yu. M. Lomov ◽  
N. R. Telesmanich ◽  
I. T. Andrusenko ◽  
E. A. Moskvitina ◽  
O. A. Areshina

The review deals with the properties of Vibrio cholerae (classical, El Tor, 0139, non-01/non-0139 strains) circulating worldwide during the seventh cholera pandemic. Particular attention is given to the variability in the cholera pathogen: the replacement of classical Vibrio cholerae by the El Tor biotype and subsequently the emergence of serogroup Vibrio cholerae 0139 and genetically altered El Tor Vibrio cholerae; the causes giving rise to these changes and spread of Vibrio cholera in the countries of the Asian continent. A large genetic variability found in Asian strains suggests that there is a real possibility of the emergence of new clones with new properties, including those with an epidemic potential. The Vibrio cholerae strains, that periodically appear in Asia and have an epidemic potential and new properties, spread over all continents, by causing cholera infection. The cholera pathogen adapts to new existence conditions in some cases, by altering some properties and, by having been rooted in a certain area, causes mainly sporadic cases of the disease. These Vibrio cholerae strains, unlike the Asian strains (the pathogens of the seventh pandemic), may be virulent, by preserving the virulence genes in the genome; however, they are, in most cases, non-endemic and unable to spread widely.

2020 ◽  
Vol 48 (6) ◽  
pp. 030006052093345
Author(s):  
Jie Chen ◽  
Jian Huang ◽  
Meirong Huang ◽  
Zehui Chen ◽  
Anlin Chen ◽  
...  

In recent decades, increasing numbers of human infections have been linked to non-O1/non-O139 Vibrio cholerae. Septicemia resulting from non-O1/non-O139 V. cholerae infection is rare but has high mortality. The pathogenesis of non-O1/non-O139 V. cholerae septicemia is poorly understood. Here, we report two sporadic cases of septicemia following non-O1/non-O139 V. cholerae infection from an inland area of China. Patient 1 died rapidly within 24 hours, while patient 2 gradually recovered from septic shock. To explore the reasons for these divergent outcomes, we compared the two cases, tested the antibiotic sensitivity of the two isolates, and investigated their virulence genes and sequence types.


1999 ◽  
Vol 181 (14) ◽  
pp. 4250-4256 ◽  
Author(s):  
Gabriela Kovacikova ◽  
Karen Skorupski

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.


Author(s):  
Ajanta Sharma ◽  
Bornali Sarmah Dutta ◽  
Debajit Rabha ◽  
Elmy Samsun Rasul ◽  
Naba Kumar Hazarika

Background and Objectives: Information on the genetic epidemiology of cholera in Assam, a northeastern state of India is lacking despite cholera being a major public health problem. The study aimed to determine the virulence genes and genes encoding antibiotic resistance in Vibrio cholerae isolates and to determine the prevalent genotypes based on the presence or absence of the virulence genes and ctxB genotype. Materials and Methods: Twenty-five V. cholerae strains were subjected to conventional biotyping and serotyping followed by multiplex PCR to detect ctxA, ctxB, zot, ace, O1rfb, tcpA, ompU, ompW, rtxC, hly and toxR and antibiotic resistance genes. Cholera toxin B (ctxB) gene was amplified followed by sequencing. Results: All the V. cholerae O1 isolates were El Tor Ogawa and showed the presence of the core toxin region representing the genome of the filamentous bacteriophage CTXø. The complete cassette of virulence genes was seen in 48% of the isolates which was the predominant genotype. All the isolates possessed amino acid sequences identical to the El Tor ctxB subunit of genotype 3. sulII gene was detected in 68% of the isolates, dfrA1 in 88%, strB in 48% and SXT gene was detected in 36% of the isolates. Conclusion: Toxigenic V. cholerae O1 El Tor Ogawa strains of ctxB genotype 3 carrying a large pool of virulence genes are prevailing in Assam. Presence of a transmissible genetic element SXT in 36% of the strains is of major concern as it indicates the emergence of multiple drug resistance among the V. cholerae isolates.  


2001 ◽  
Vol 69 (3) ◽  
pp. 1947-1952 ◽  
Author(s):  
David K. R. Karaolis ◽  
Ruiting Lan ◽  
James B. Kaper ◽  
Peter R. Reeves

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.


2020 ◽  
Author(s):  
Stefan L Nordqvist ◽  
Kaisa Thorell ◽  
Frida Nilsson ◽  
Madeleine Löfstrand ◽  
Arvid Hagelberg ◽  
...  

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.


2014 ◽  
Vol 3 (1) ◽  
Author(s):  
Racheal W. Kimani ◽  
Anne W. T. Muigai ◽  
Willie Sang ◽  
John N. Kiiru ◽  
Samuel Kariuki

Background: Since 1971, Kenya has had repeated cholera outbreaks. However, the cause of seasonal epidemics of cholera is not fully understood and neither are the factors that drive epidemics, both in Kenya and globally.Objectives: The objectives of the study were to determine the environmental reservoirs of V. cholerae during an interepidemic period in Kenya and to characterise their virulence factors.Methods: One hundred (50 clinical, 50 environmental) samples were tested for V. cholerae isolates using both simplex and multiplex polymerase chain reaction.Results: Both sediments and algae from fishing and landing bays yielded isolates of V. cholerae. Clinical strains were characterised along with the environmental strains for comparison. All clinical strains harboured ctxA, tcpA (El Tor), ompU, zot, ace, toxR, hylA (El Tor) and tcpI genes. Prevalence for virulence genes in environmental strains was hylA (El Tor) (10%), toxR (24%), zot (22%), ctxA (12%),tcpI (8%), hylA (26%) and tcpA (12%).Conclusion: The study sites, including landing bays and beaches, contained environmental V. cholerae, suggesting that these may be reservoirs for frequent epidemics. Improved hygiene and fish-handling techniques will be important in reducing the persistence of reservoirs.


2002 ◽  
Vol 70 (5) ◽  
pp. 2441-2453 ◽  
Author(s):  
Manrong Li ◽  
Toshio Shimada ◽  
J. Glenn Morris ◽  
Alexander Sulakvelidze ◽  
Shanmuga Sozhamannan

ABSTRACT 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 ∼23.4-kb gene cluster had replaced all but the ∼4.2-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 CTXφ; the O27 strain possessed a CTXφ with a recently reported immune specificity (rstR-4** allele) and a novel ctxB allele, and the O37 strain had an El Tor CTXφ (rstRET allele) and novel ctxAB alleles. Although the O53 and O65 strains lacked the ctxAB genes, they carried a pre-CTXφ (i.e., rstRcla ). 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.


Author(s):  
Tarh, Jacqueline Ebob ◽  
C. I. Mboto ◽  
B. E. E. Asikong ◽  
Iroegbu Christian Ukwuoma

Indeed, a host of the plenty of reports about pathogenic Vibrios, have been from African researchers. And they assert that this severe diarrhea causing agent originated from Asia thousands of years ago and spread (first, via the sea route) affecting particularly the coastal towns and fishing villages, before moving to other parts of the world. Following the primary cholera outbreak of 1868, Vibrio cholera, appeared in the Atlantic coast of West Africa. The pathogen then invaded African countries chronologically beginning with Guinea, then Sierra Leone, Liberia, Cote d’ivoire, Mali, Togo, Dahomey, Upper Volt (Burki Na-faso) and finally Nigeria (Lagos) and Niger in December, 1970. Various serogroups (O139 and O1 with biotypes Classical and El Tor) and Serotypes of O1 (Ogawa, Inaba and Hikojima) and recently, the O395 strain have been reported; especially from outbreaks reported from hotspots that are close to riverine areas. This suggests that these emergent pathogenic species originate from around water environments probably from the non-pathogenic strains. This condition is likely harnessed by Lateral Gene Transfer (LGT), which is seen to occur usually between pandemic V. cholerae and environmental strains; a situation that may result in the creation of new pandemic strains. Therefore, in order to better understand and appreciate the evolution of the Vibrio cholerae strains that are involved in epidemics, and the relationship between the species causing particular epidemics in different regions of Africa, a study of the molecular picture of the environmental strains and the mechanisms by which the pathogenic Vibrio cholera strains appear and diffuse from these strains is necessary. This review seeks to trace the origin and spread route of Vibrio cholerae strains causing epidemics in different regions of the African continent (Nigeria in particular) with the aim of establishing relationships between the strains causing epidemics in these regions. This will help in the development of better intervention strategies to contain the disease.


1999 ◽  
Vol 67 (10) ◽  
pp. 5117-5123 ◽  
Author(s):  
Yvette M. Murley ◽  
Patricia A. Carroll ◽  
Karen Skorupski ◽  
Ronald K. Taylor ◽  
Stephen B. Calderwood

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.


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