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Enteroinvasive (EIEC) and are closely related agents of bacillary dysentery. It is widely viewed that EIEC and species evolved from via independent acquisitions of a large virulence plasmid (pINV) encoding a type 3 secretion system (T3SS). Sequence Type (ST)99 O96:H19 is a novel clone of EIEC responsible for recent outbreaks in Europe and South America. Here, we use 92 whole genome sequences to reconstruct a dated phylogeny of ST99 , revealing distinct phylogenomic clusters of pINV-positive and -negative isolates. To study the impact of pINV acquisition on the virulence of this clone, we developed an EIEC-zebrafish infection model showing that virulence of ST99 EIEC is thermoregulated. Strikingly, zebrafish infection using a T3SS-deficient ST99 EIEC strain and the oldest available pINV-negative isolate reveals a separate, temperature-independent mechanism of virulence, indicating that ST99 non-EIEC strains were virulent before pINV acquisition. Taken together, these results suggest that an already pathogenic acquired pINV and that virulence of ST99 isolates became thermoregulated once pINV was acquired. IMPORTANCE Enteroinvasive (EIEC) and are etiological agents of bacillary dysentery. Sequence Type (ST)99 is a clone of EIEC hypothesized to cause human disease by the recent acquisition of pINV, a large plasmid encoding a type 3 secretion system (T3SS) that confers the ability to invade human cells. Using Bayesian analysis and zebrafish larvae infection, we show that the virulence of ST99 EIEC isolates is highly dependent on temperature, while T3SS-deficient isolates encode a separate temperature-independent mechanism of virulence. These results indicate that ST99 non-EIEC isolates may have been virulent before pINV acquisition and highlight an important role of pINV acquisition in the dispersal of ST99 EIEC in humans, allowing wider dissemination across Europe and South America.
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http://dx.doi.org/10.1128/mbio.00882-23 | DOI Listing |
Microorganisms
June 2023
Host-Microbe Interactions Laboratory, Centre for Chemical and Synthetic Biology, Department of Chemistry and Biomolecular Sciences, University of Ottawa, Ottawa, ON K1N 6N5, Canada.
spp. cause hundreds of millions of intestinal infections each year. They target the mucosa of the human colon and are an important model of intracellular bacterial pathogenesis.
View Article and Find Full Text PDFmBio
August 2023
Department of Infection Biology, London School of Hygiene and Tropical Medicine, London, United Kingdom.
Microb Genom
June 2022
Department of Molecular Medicine, Sapienza University of Rome, Rome, Italy.
is a major health burden in low- and middle-income countries, where it is a leading cause of mortality associated with diarrhoea in children, and shows an increasing incidence among travellers and men having sex with men. Like all spp., has evolved from commensal following the acquisition of a large plasmid pINV, which contains genes essential for virulence.
View Article and Find Full Text PDFFront Microbiol
December 2017
Istituto Pasteur Italia, Department of Biology and Biotechnology "C. Darwin", Sapienza Università di Roma, Rome, Italy.
Among the intestinal pathogenic , enteroinvasive (EIEC) are a group of intracellular pathogens able to enter epithelial cells of colon, multiplicate within them, and move between adjacent cells with a mechanism similar to , the ethiological agent of bacillary dysentery. Despite EIEC belong to the same pathotype of , they neither have the full set of traits that define nor have undergone the extensive gene decay observed in . Molecular analysis confirms that EIEC are widely distributed among phylogenetic groups and correspond to bioserotypes found in many serogroups.
View Article and Find Full Text PDFPLoS Genet
September 2017
Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
Acquisition of a single copy, large virulence plasmid, pINV, led to the emergence of Shigella spp. from Escherichia coli. The plasmid encodes a Type III secretion system (T3SS) on a 30 kb pathogenicity island (PAI), and is maintained in a bacterial population through a series of toxin:antitoxin (TA) systems which mediate post-segregational killing (PSK).
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