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A Case Of Vero Cytotoxinproducing Escherichia Coli (VTEC)
Published in Meera Chand, John Holton, Case Studies in Infection Control, 2018
In addition to the production of VT, strains causing severe disease are able to attach to the host gut mucosa via one of two known attachment mechanisms. The most common mechanism involves a system of type III secreted proteins, encoded by genes on a pathogenicity island called the locus of enterocyte effacement, that mediate intimate attachment to the gut enterocytes and destroy the microvilli surrounding the point of attachment. A second attachment mechanism has recently been described in strains of VTEC harbouring plasmid-encoded genes that facilitate the aggregative attachment of the bacteria to the gut, including the aggregative adherence regulator (aggR), aggregative adherence transporter (aat), and aggregative fimbriae.
Engineering Escherichia coli to Combat Cancer
Published in Ananda M. Chakrabarty, Arsénio M. Fialho, Microbial Infections and Cancer Therapy, 2019
Carlos Piñero-Lambea, David Ruano-Gallego, Gustavo Bodelón, Beatriz Álvarez, Luis Ángel Fernández
We chose the filamentous injectisomes of EPEC for expression in E. coli K-12 because of their distinctive properties (i.e., extracellular injection and long filament) and demonstrated the capacity to translocate antibody fragments [81]. The assembly of EPEC injectisomes and their encoding genes are well characterized [94]. Other EPEC-related pathogens, such as EHEC and Citrobacter rodentium, also encode similar filamentous injectisomes. These bacteria form part of the attaching and effacing (A/E) family of enteric pathogens causing diarrheal diseases [75, 95, 96]. These bacteria infect the small and large intestines of humans and animals, causing A/E lesions characterized by the intimate attachment of the bacteria to the enterocytes and the disruption (effacement) of the absorptive microvilli surface [97, 98]. All genes required for the assembly of the T3SS injectisome of EPEC and other A/E pathogens are present in the locus for enterocyte effacement (LEE) island [88], a genomic locus organized in five main operons and other smaller transcriptional units. Twenty-seven proteins encoded in the LEE participate in the assembly of the filamentous injectisomes of EPEC, including chaperones and proteins regulating injection [94]. This complexity has hindered the transfer of all genes required for assembly of EPEC injectisomes in E. coli K-12. In a previous study, the whole LEE of EPEC was cloned in E. coli K-12 in a cosmid but resulted in poor assembly of the T3SS [88]. Hence, we assessed the possibility of engineering an E. coli K-12 strain expressing functional injectisomes from EPEC using a synthetic approach.
Escherichia
Published in Dongyou Liu, Laboratory Models for Foodborne Infections, 2017
EHEC is characterized by the production of Shiga toxins (Stx1 and/or Stx2, leading to its alternative name of STEC) and the formation of A/E lesion, notably in the cecum and ascending colon [14–16]. EHEC typically causes an afebrile bloody colitis (bloody stools with ulcerations of the bowel) known as hemorrhagic colitis (HC), which is characterized by the sudden onset of abdominal pain, severe cramps, and diarrhea within 24 h. In about 10% of patients (e.g., children and the elderly), infection with EHEC O157 may result in HUS, which is defined by acute renal failure, hemolytic anemia, and thrombocytopenia. Colonoscopy examination reveals the presence of edema, erythema (redness), hemorrhage, erosion, and, occasionally, a long ulcer-like lesion, with a marked narrowing of the luminal space. Histologic examination indicates destruction of the surface epithelium, neutrophil infiltration of the lamina propria, and the formation of crypt abscesses. In patients (especially children of <5 years of age and the elderly) with diarrhea and HUS, renal pathology consists of endothelial swelling and glomerular thrombosis with congested rather than ischemic glomeruli. The most prevalent EHEC serotype causing outbreaks in North America and other parts of the world is O157:H7 [17,18]. Besides Shiga toxin, which may account for the severe complications including HUS, O157:H7 expresses several other virulence factors including intimin, translocated intimin receptor (Tir), a T3SS, and enterohemolysin [19]. The genes encoding many of these factors are located on a 44 kb pathogenicity island (also known as the locus of enterocyte effacement or the LEE locus) [20–22]. Cattle act as a primary reservoir for EHEC, although vegetables (lettuce, spinach, and sprouts) and fruits may also serve as vehicles for EHEC outbreaks [23].
Salmonella enterica subsp. II serovar 4,5,12:a:- may cause gastroenteritis infections in humans
Published in Gut Microbes, 2022
Meiying Yan, Yongming Zhou, Yang Cao, Zhenpeng Li, Xin Lu, Bo Pang, Shukun Wang, Biao Kan
SPIs 1–3, 5, 6, 9, 11, 12, 16 and 19 and the partial genes of SPI-18 and hlyE were present in all S. 4,5,12:a:- strains. All SPI-1 and SPI-2 genes and 10 effectors, including sipA, sipB, sipC, sopA, sopD, sopE2, and sptP, translocated by the SPI-1 type 3 secretion system (T3SS) were also detected in these strains. Similarly, most of the SPI-2 translocated effectors, including spiC, sseF, sseG, sifA, sifB, sspH2, sseJ, sseL, sseK2 and pipB2, were present in the strains. However, other effectors including avrA, sopB, sopE, slrP, sspH1, sopD2, sopF, sseK1, sseK3, gogB, pipB, and sseI were absent in these strains. Universal fimbrial clusters (bcf, csg, fim, stb, and sth), one ‘typhoid’ fimbrial operon sta, and an invasion gene pagN were present in the genomes of these strains. Some nonfimbrial adherence determinants, including misL, ratB, and sinH, were also present. Other virulence genes, such as phoPQ, mig14, and mgtBC, were also found. Additionally, the locus of enterocyte effacement (LEE) of E. coli O157:H7,21 and ACE T6SS of E. coli were found in these strains, as well as eae and usp.
Indole intercepts the communication between enteropathogenic E. coli and Vibrio cholerae
Published in Gut Microbes, 2022
Orna Gorelik, Alona Rogad, Lara Holoidovsky, Michael M. Meijler, Neta Sal-Man
EPEC relies on the type III secretion system (T3SS) to infect host cells.10 The T3SS is a large protein transport complex that many other pathogenic gram-negative bacteria use to form a nano-syringe structure. The T3SS translocates effectors directly into host cells, where they interfere with crucial cellular processes that ultimately promote bacterial replication and transmission.11–13 In EPEC, the T3SS is encoded on a large 35-kbp chromosomal pathogenicity island, known as the locus of enterocyte effacement (LEE).14 The LEE consists of 41 genes, organized in seven operons (LEE1–LEE7), that encode structural proteins, regulators, and effector proteins.13,15,16 We discovered that EPEC T3SS activity, and hence its infection ability, are enhanced in response to CAI-1.7
Virulence-related O islands in enterohemorrhagic Escherichia coli O157:H7
Published in Gut Microbes, 2021
Lingyan Jiang, Wen Yang, Xinlei Jiang, Ting Yao, Lu Wang, Bin Yang
Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is an important human pathogen that specifically colonizes the large intestine, causing disease.1, 2 Shiga toxins (Stxs), which are the major virulence factors of EHEC O157:H7, are known to cause damage to a variety of cell types and have often been associated with hemorrhagic colitis (HC) and the lethal hemolytic uremic syndrome (HUS) in humans.3,4 The pathogenesis of EHEC O157:H7 infections is characterized by the formation of an attaching and effacing (A/E) lesion that involves the intimate attachment of bacteria to the host enterocyte membrane, the subversion of actin and cytoskeletal components, and the formation of a pedestal structure beneath the adherent bacteria.5,6 The ability of EHEC O157:H7 to form A/E lesions is conferred by a large pathogenicity island, termed locus of enterocyte effacement (LEE), which consists of five polycistronic operons (LEE1 to LEE5).7 In particular, LEE encodes a type III secretion system (T3SS) that exports effector molecules, including the intimin adhesin, the translocated intimin receptor (Tir), and several secreted proteins (Esp), which are important in the modification of the host cell signal transduction during the formation of A/E lesions.1,8