scholarly journals A Rough Variant of Nontoxigenic Vibrio Cholerae O139 Imported From Vietnam

2021 ◽  
Author(s):  
Pontus Westerström ◽  
Ulrik Bak Dragsted
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Virulence Genes ◽  
Research Question ◽  
Membrane Properties ◽  
Rare Finding ◽  
Mild Disease ◽  
Asian Strain ◽  
Vibrio Cholerae O139 ◽  
Different Strains

Abstract Purpose (stating the main purposes and research question)Vibrio cholerae is classified in O-antigen polysaccharide outer membrane properties where O1 and O139 are strains that cause pandemics and epidemics while non-O1/non-O139 usually cause mild disease. The dynamic evolution of Vibrio cholerae involves new virulence factors through horizontal gene transfer and formerly nontoxigenic serogroups are being reported as causing increasingly severe forms of human disease. Our purpose was to investigate serogroup and virulence factors in one imported isolate from Vietnam and compare these to virulence factors seen in different strains of Vibrio cholerae.MethodsWe have serotyped one isolate of imported Vibrio cholerae from Vietnam to Denmark and performed whole genome sequencing to identify known virulence genes. ResultsWe have identified virulence factors in our isolate that are recently discovered and one toxin, MakA, has not previously been reported from an Asian strain. The isolate was found to be a serogroup non-O1/non-O139 strain, however, sequence analysis gave a 96, 6% ID match of the wbfZ gene, stipulating our isolate to belong to either serogroup O22 or O139. ConclusionsLooking at the combination of virulence factors of the isolate we suggest the finding of a rough variant of a nontoxigenic Vibrio cholerae O139 rather than a O22 serogroup version. This is a rare finding in a clinical isolate.

scholarly journals Origins of pandemic Vibrio cholerae from environmental gene pools

2016 ◽  
Author(s):  
B. Jesse Shapiro ◽  
Inès Levade ◽  
Gabriela Kovacikova ◽  
Ronald K. Taylor ◽  
Salvador Almagro-Moreno
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Virulence Genes ◽  
Mammalian Host ◽  
Comparative Genomic ◽  
Gene Pools ◽  
Host Colonization ◽  
Bacterial Populations ◽  
Genomic Features ◽  
Clinical Strains

AbstractSome microbes can transition from an environmental lifestyle to a pathogenic one1–3. This ecological switch typically occurs through the acquisition of horizontally acquired virulence genes4,5. However, the genomic features that must be present in a population prior to the acquisition of virulence genes and emergence of pathogenic clones remain unknown. We hypothesized that virulence adaptive polymorphisms (VAPs) circulate in environmental populations and are required for this transition. We developed a comparative genomic framework for identifying VAPs, using Vibrio cholerae as a model. We then characterized several environmental VAP alleles to show that, while some of them reduced the ability of clinical strains to colonize a mammalian host, other alleles conferred efficient host colonization. These results show that VAPs are present in environmental bacterial populations prior to the emergence of virulent clones. We propose a scenario in which VAPs circulate in the environment, they become selected and enriched under certain ecologicalconditions, and finally a genomic background containing several VAPs acquires virulence factors that allows for its emergence as a pathogenic clone.

scholarly journals Virulence factors in environmental and clinical Vibrio cholerae from endemic areas in Kenya

2014 ◽  
Vol 3 (1) ◽  
Author(s):  
Racheal W. Kimani ◽  
Anne W. T. Muigai ◽  
Willie Sang ◽  
John N. Kiiru ◽  
Samuel Kariuki
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Environmental Samples ◽  
Virulence Genes ◽  
Clinical Strains ◽  
Seasonal Epidemics ◽  
Polymerase Chain ◽  
Endemic Areas ◽  
Study Sites ◽  
El Tor

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.

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 Classical and El Tor Biotypes of Vibrio cholerae Differ in Timing of Transcription of tcpPHduring Growth in Inducing Conditions

2000 ◽  
Vol 68 (5) ◽  
pp. 3010-3014 ◽  
Author(s):  
Yvette M. Murley ◽  
Jaideep Behari ◽  
Robert Griffin ◽  
Stephen B. Calderwood
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Virulence Genes ◽  
Phase Growth ◽  
Classical Strain ◽  
The Absolute ◽  
The Difference ◽  
El Tor ◽  
Transcriptional Fusions

ABSTRACT Two protein pairs in Vibrio cholerae, ToxRS and TcpPH, are necessary for transcription from the toxT promoter and subsequent expression of cholera virulence genes. We have previously shown that transcription of tcpPH in classical strains ofV. cholerae is activated at mid-log-phase growth in ToxR-inducing conditions, while transcription of tcpPH in El Tor strains is not. In this study, we showed that while transcription of tcpPH differs at mid-log-phase growth in ToxR-inducing conditions between the biotypes, transcription is equivalently high during growth in AKI conditions. We usedtcpPH::gusA transcriptional fusions to quantitate expression of tcpPH in each biotype throughout growth in ToxR-inducing conditions and showed that although transcription of tcpPH is reduced at mid-log-phase growth in an El Tor strain, transcription is turned on later in growth to levels in excess of those in the classical strain (although cholera toxin is not produced). This suggests that the difference in expression of cholera virulence factors in response to ToxR-inducing conditions between the El Tor and classical biotypes of V. choleraemay be related to the timing of transcription of tcpPHrather than the absolute levels of transcription.

scholarly journals The Vibrio cholerae O139 Calcutta Bacteriophage CTXφ Is Infectious and Encodes a Novel Repressor

1999 ◽  
Vol 181 (21) ◽  
pp. 6779-6787 ◽  
Author(s):  
Brigid M. Davis ◽  
Harvey H. Kimsey ◽  
William Chang ◽  
Matthew K. Waldor
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Inhibitory Effect ◽  
Genes Encoding ◽  
Vibrio Cholerae O139 ◽  
Allele Specific ◽  
Toxigenic Strains ◽  
El Tor ◽  
Novel Allele

ABSTRACT CTXφ is a lysogenic, filamentous bacteriophage. Its genome includes the genes encoding cholera toxin (ctxAB), one of the principal virulence factors of Vibrio cholerae; consequently, nonpathogenic strains of V. cholerae can be converted into toxigenic strains by CTXφ infection. O139 Calcutta strains of V. cholerae, which were linked to cholera outbreaks in Calcutta, India, in 1996, are novel pathogenic strains that carry two distinct CTX prophages integrated in tandem: CTXET, the prophage previously characterized within El Tor strains, and a new CTX Calcutta prophage (CTXcalc). We found that the CTXcalc prophage gives rise to infectious virions; thus, CTXETφ is no longer the only known vector for transmission of ctxAB. The most functionally significant differences between the nucleotide sequences of CTXcalcφ and CTXETφ are located within the phages’ repressor genes (rstR calc andrstR ET, respectively) and their RstR operators. RstRcalc is a novel, allele-specific repressor that regulates replication of CTXcalcφ by inhibiting the activity of the rstA calc promoter. RstRcalc has no inhibitory effect upon the classical and El Tor rstA promoters, which are instead regulated by their cognate RstRs. Consequently, production of RstRcalc renders a CTXcalc lysogen immune to superinfection by CTXcalcφ but susceptible (heteroimmune) to infection by CTXETφ. Analysis of the prophage arrays generated by sequentially integrated CTX phages revealed that pathogenic V. cholerae O139 Calcutta probably arose via infection of an O139 CTXETφ lysogen by CTXcalcφ.

Molecular Subtyping Of Toxigenic Vibrio Cholerae O139 Causing Epidemic Cholera In India And Bangladesh, 1992-1993

1995 ◽  
Vol 171 (1) ◽  
pp. 122-127 ◽  
Author(s):  
T. Popovic ◽  
P. I. Fields ◽  
O. Olsvik ◽  
J. G. Wells ◽  
G. M. Evins ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Molecular Subtyping ◽  
Vibrio Cholerae O139

scholarly journals Molecular characterization of virulence factors in Staphylococcus aureus isolated from bovine subclinical mastitis in central Ethiopia

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Desiye Tesfaye Tegegne ◽  
Gezahegne Mamo ◽  
Hika Waktole ◽  
Yohannes Equar Messele
Keyword(s):  
Staphylococcus Aureus ◽  
Dairy Cows ◽  
Virulence Factors ◽  
Virulence Genes ◽  
Animal Health ◽  
Subclinical Mastitis ◽  
Biochemical Tests ◽  
Milk Samples ◽  
Lactating Dairy Cows ◽  
Genomic Study

Abstract Purpose Staphylococcus aureus (S. aureus) is the most important pathogen involved in bovine mastitis in dairy production. S. aureus produces a spectrum of extracellular protein toxins and virulence factors which are thought to contribute to the pathogenicity of the organism. The aim of this work was to isolate and molecular characterize S. aureus associated with bovine subclinical mastitis in the central part of Ethiopia. Methods A total of 265 lactating dairy cows from various dairy farms in four different geographical locations were screened by the California mastitis test (CMT) for bovine subclinical mastitis. One hundred thirty CMT-positive milk samples were collected and transported to the laboratory. Different biochemical tests and polymerase chain reaction (PCR) were used for the identification of S. aureus isolates. Finally, PCR was performed for molecular detection of virulence genes. Results From a total of 265 lactating dairy cows screened, 49% (n = 130) were positive for bovine subclinical mastitis. One hundred thirty mastitic milk samples were subjected to bacterial culturing, and one hundred (76%) S. aureus isolates were identified based on phenotypic characters. Sixty-eight confirmed S. aureus isolates were obtained using PCR. The confirmed S. aureus isolates were tested for six virulence genes (tsst-1, hlb, eta, sea, clfA, and icaD) using PCR. Of the six virulence genes screened from all the isolates, only two (clfA and eta) were detected in the isolates. Out of 68 isolates, 25% and 22% were possessed the eta and clfA genes, respectively. Conclusion The presence of Staphylococcus aureus having virulence genes (eta and clfA) revealed that mastitis is a major concern nowadays affecting animal health, milk quality, and yield. Further genomic study of these isolates will provide broad new insights on virulence.

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.

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