Accessory Toxins of Vibrio Pathogens and Their Role in Epithelial Disruption During Infection

Pérez-Reytor, Diliana; Jaña, Víctor; Pavéz, Leonardo; Navarrete, Paola; García, Katherine

doi:10.3389/fmicb.2018.02248

Cited by 46 publications

(50 citation statements)

References 96 publications

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“…For instance, CTXΦ is able to transduce the cholera toxin (CT) from V. cholera to V. mimicus leading to the emergence of a pathogenic V. mimicus form (58, 59). Many vibriophages contain virulence genes responsible for severe gastro-intestinal diseases (47, 48). For instance, almost 80% of clinical V. parahaemolyticus strains contain filamentous phages, encoding the zona occludens toxin (Zot) (22).…”

Section: Discussionmentioning

confidence: 99%

“…We found that one of the active filamentous phages (i.e. Vibrio phage VALGΦ6) contains the virulence cassette comprising the Zot and the Ace proteins, which is frequently found in vibriophages and responsible for severe gastro-intestinal diseases (47, 48). To compare these two proteins with other Zot and Ace proteins isolated from various vibriophages we generated protein alignments using AliView (40) and examined the presence of Walker A and Walker B motifs in Vibrio phage VALGΦ6 Zot proteins.…”

Section: Methodsmentioning

confidence: 99%

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Closely relatedVibrio alginolyticusstrains encode an identical repertoire of prophages and filamentous phages

Chibani

Hertel

Hoppert

et al. 2019

Preprint

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Filamentous vibriophages represent a massive repertoire of virulence factors which can be transferred across species boundaries, leading to the emergence of deadly pathogens. All filamentous vibriophages that were characterized until today were isolated from human pathogens. Considering frequent horizontal gene transfer among vibrios, we predict that other environmental isolates, including non-human pathogens also carry filamentous phages, of which some may encode virulence factors.The aim of this study was to characterize the phage repertoire, consisting of prophages and filamentous phages, of a marine pathogen, Vibrio alginolyticus. To do so, we sequenced eight different V. alginolyticus strains, isolated from different pipefish and characterised their phage repertoire using a combination of morphological analyses and comparative genomics.We were able to identify a total of five novel phage regions (three different Caudovirales and two different Inoviridae), whereby only those two loci predicted to correspond to filamentous phages (family Inoviridae) represent actively replicating phages. Unique for this study was that all eight host strains, which were isolated from different eukaryotic hosts have identical bacteriophages, suggesting a clonal expansion of this strain after the phages had been acquired by a common ancestor. We further found that co-occurrence of two different filamentous phages leads to within-host competition resulting in reduced phage replication by one of the two phages. One of the two filamentous phages encoded two virulence genes (Ace and Zot), homologous to those encoded on the V. cholerae phage CTXΦ. The coverage of these zot-encoding phages correlated positively with virulence (measured in controlled infection experiments on the eukaryotic host), suggesting that this phages is an important virulence determinant.Impact statementMany bacteria of the genus Vibrio, such as V. cholerae or V. parahaemolyticus impose a strong threat to human health. Often, small viruses, known as filamentous phages encode virulence genes. Upon infecting a bacterial cell, these phages can transform a previously harmless bacterium into a deadly pathogen. While filamentous phages and their virulence factors are well-characterized for human pathogenic vibrios, filamentous phages of marine vibrios, pathogenic for a wide range of marine organisms, are predicted to carry virulence factors, but have so far not been characterized in depth. Using whole genome sequencing and comparative genomics of phages isolated from a marine fish pathogen V. alginolyticus, we show that also environmental strains harbour filamentous phages that carry virulence genes. These phages were most likely acquired from other vibrios by a process known as horizontal gene transfer. We found that these phages are identical across eight different pathogenic V. alginolyticus strains, suggesting that they have been acquired by a common ancestor before a clonal expansion of this ecotype took place. The phages characterized in this study have not been described before and are unique for the Kiel V. alginolyticus ecotype.Data SummaryThe GenBank accession numbers for all genomic sequence data analysed in the present study can be found in Table S1.All phage regions identified by PHASTER analysis of each chromosome and the respective coverage of active phage loci are listed in Table S2.GenBank files were deposited at NCBI for the two actively replicating filamentous phages VALGΦ6 (Accession number: MN719123) and VALGΦ8 (Accession number: MN690600)The virulence data from the infection experiments have been deposited at PANGAEA: Accession number will be provided upon acceptance of the manuscript.Data statementAll supporting data have been provided within the article or through supplementary data files. Four supplementary tables and six supplementary figures are available with the online version of this article.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Closely relatedVibrio alginolyticusstrains encode an identical repertoire of prophages and filamentous phages

Chibani

Hertel

Hoppert

et al. 2019

Preprint

View full text Add to dashboard Cite

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“…The gut lumen contains 10 3 -10 11 bacteria/ml, [63] that in aggregate contain 1 g or more of endotoxin, that if purified and intravenously injected could be fatal to hundreds or even thousands of humans [64]. Endotoxins activate specific membrane receptors termed Toll-like receptors that are members of a class of pro-inflammatory receptors hat recognize pro-inflammatory molecules termed "patternassociated molecular patterns" or PAMPS that in turn can activate genes that initiate inflammatory cascades in the host [49,65]. Parenteral administration of minute amounts of endotoxins to humans elicits an inflammatory reaction typical of SIRS (fever or hypothermia, tachycardia, hyperpnea, leukocytosis, and hypotension), whereas larger amounts of administered endotoxins typically produce sepsis and shock [66,67].…”

Section: Pathologic Consequences Of Bt and Endotoxin Transportmentioning

confidence: 99%

The “Leaky Gut”: Tight Junctions but Loose Associations?

2019

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“…This is a pentameric toxin that triggers signals for elevation of intracellular cAMP and consequently, stimulates luminal secretion of electrolytes and water from enterocytes. This is the basis of loss of water and electrolytes from the gut, weight loss, dehydration and death [46,47].…”

Section: Amongmentioning

confidence: 99%

“…Furthermore, the intestinal cells are stimulated by the Accesory cholera enterotoxin (ACE), to secrete Ca 2+dependent Cl -/HCO3 -, while the Heat stable enterotoxin (Sta) causes increased cGMP secretion and inhibition of the regulatory mechanism of Na + /Cl. These thus lead to an efflux of water and electrolytes (sodium and chloride ions) into the gut lumen, causing the profuse watery diarrhoeal characteristic seen in cholera disease [46].…”

Section: Cholera Toxin (Choleragen) and Its Mechanism Of Actionmentioning

confidence: 99%

Epidemiological Distribution of Different Vibrio cholerae Strains Causing Cholera Disease in Endemic Countries: A Review

Ebob

2019

JAMMR

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Cholera is an acute severe watery diarrhoeal disease caused by a toxigenic strains of Vibrio cholerae. Significant clinical presentations characteristic of this disease include; asymptomatic intestinal colonization, accompanied by rapid fluid and electrolyte loss, cholera sicca (unusual accumulation of fluid in the intestinal lumen leading to circulatory collapse and death), significant hypovolemia and electrolyte abnormalities, abdominal pain and discomfort, borborygmi, and vomiting. However, diagnostic pointers like hypokalemia, hypo or hypernatremia, isonatremic dehydration, hypocalcemia, and acidosis may be seen. Yet, in complicated cases, Kidney failure with acute tubular necrosis due to anuria, low glycogen, inadequate gluconeogenesis, severe hypoglycemia, coma (in rare occasions), chronic enteropathy, malnutrition and pneumonia in children may occur. Since man is the natural host of this pathogenic bacterium (Vibio cholera), which he sheds into the environment through faeces or vomitus, its eradication has become difficult especially from their natural warm aquatic environmental reservoirs. The association of this disease with drinking water, and food, has been traced to the pollution of water sources (wells, rivers, streams and ponds) as well as food sources like vegetables (from gardens which are watered with sewage contaminated water from the environment). Cholera has become a night mare especially in continents like Asia and Africa, which lack adequate healthcare facilities and infrastructures. These areas represent the most endemic regions of the nearly 50 countries recorded to be endemic to cholera in the world. The World Health Organization reports that only an estimated 5–10% of the actual case number are officially reported annually worldwide. This review attempts to describe the epidemiological distribution of the various strains of Vibrio cholerae causing epidemics all over the globe.

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Accessory Toxins of Vibrio Pathogens and Their Role in Epithelial Disruption During Infection

Cited by 46 publications

References 96 publications

Closely relatedVibrio alginolyticusstrains encode an identical repertoire of prophages and filamentous phages

Closely relatedVibrio alginolyticusstrains encode an identical repertoire of prophages and filamentous phages

The “Leaky Gut”: Tight Junctions but Loose Associations?

Epidemiological Distribution of Different Vibrio cholerae Strains Causing Cholera Disease in Endemic Countries: A Review

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