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Both pathogenic and non-pathogenic types of E. coli have evolved through a complex process. The ancestral backbone genes that define E. coli have undergo slow accumulation of vertically acquired sequence changes, but genes in the remainder of the chromosome are, in a relative sense, newly introduced via numerous, independent horizontal gene transfer events at many discrete sites, some serving an universal insertion targets used independently in separate lineages. The net result is a mosaic genome structure in which newly acquired genes in each of the E. coli types are placed into a framework made of genes that distinguishes E. coli from its closer relatives.
For uropathogenic strains of E. coli, island acquisition resulted in the capability to infect the urinary tract and bloodstream and evade host defences without compromising the ability to harmlessly colonize the intestine.
To begin to understand the genetic bases for pathogenicity and the evolutionary diversity of E. coli, we present here-----.
Virulence factors encoded on bacteriophages may allow the bacterium to enlarge its host fange and increase its fitness in an environmental niche by promoting evasion of host immune defences or providing mechanisms to breach host structural barriers. In support of this concept, a variety of major bacterial toxins associated with important epidemics are carried on bacteriophages.
An example of recent emergence of a pathogen with a bacteriophage encoded toxin is E. coli serotype O157:H7, which causes haemolytic-uremic syndrome in children. Virulence factors other than toxins can also be carried on bacteriophages.
Some strains of E. coli are able to cause intestinal as well as extra-intestinal infectious diseases. Urinary tract infections represent the main diseases due to extra-intestinal E. coli.
Escherichia coli O157:H7, a toxin-producing food and waterborne bacterial pathogen, has been linked to large outbreaks of gastrointestinal illness for more than two decades. E. coli O157:H7 causes a wide range of clinical illness that varies by outbreak, although factors that contribute to variation in disease severity are poorly understood. Several recent outbreaks involving O157 contamination of fresh produce were associated with more severe disease, as defined by higher haemolytic uremic syndrome and hospitalization frequencies, suggesting that increased virulence has envolved.
These findings suggest that an emergent subpopulation of the clade 8 lineage has acquired critical factors that contribute to more severe disease. The ability to detect and rapidly genotype O157 strains belonging to such linesges is important and will have a significant impact on both disease diagnosis and atreatment guidlines.
Enterohemorrhagic Escherichia coli /EHEC) includes a diverse population of shiga toxin-producing E. coli that causes outbreaks of food and waterborne disease. EHEC often resides in bovine reservoirs and is transmitted via many food vehicles including cooked meat, such as hamburger and salami, and raw vegetables, such as lettuce and spinach. It is not clear why outbreaks of EHEC O157 vary dramatically in the severity of illness and the frequency of the most serious complication, haemolytic uremic syndrome (HUS). One hypothesis is that outbreak strains differ in virulrnce as a result of variation in the presence and expression of different Shiga toxin (Stx) gene combinations.
To assess the genetic diversity and variability in virulence among E. coli O157 strains, we developed ------ for identifying .....
Although molecular subtyping methods, such as ......., reveal extensive genomic diversity among O157 outbreaks, /DNA fingerprinting data are not ameable to population genetic or phylogenetic analyses.Here we genotyped --- clinical strains of EHEC O157 based on --- that separated strains into geneticali distinct groups........ These data form a basis for addressing how EHEC O157 has diversifies and evolved in genome content and for assessing intrinsic differences among O157 lineages with regard to clinical presentation and disease severity.
RES --- Because the production of Stx has ben linked to virulence in O157 strains, we estimated the frequency of one or more of three variants (stx1, stx2, and stx2c) by clade. Although stx1 was found in more than half of 519 of the 528 O157 strains tested, the distribution is highly non-random across clades. The stx1 gene was common in clade 2 strains but not clade 8. The stx2 gene was present in virtually all O157 strains evaluated, occurring most frequently in clade 2 strains.
DIS---- The population genetics and epidemiology of E. coli O157:H7 infections have changed dramatically since the first outbreaks of illness associated with contaminated ground beef occurred in early 1980s.
The current model of emergence of toxigenic E. coli O+Å¥ý.hý from its nontoxigenetic, less virulent progenitor, E. coli 055:H7 relies on four crucial sequential events: (i) acacquisition of an stx2 bacteriophage in a single event and at a single site (probably wrbA); äii) splitting off of the clone leading to E. coli O157:H-; (iii) acquisition of the stx1 bacteriophage in a single event and at a single site (probably yehV) by e. coli O157:H7; and (iv) loss of the ability to ferment sorbitol by E. coli O157:H7 ( event iv might have preceded event iii during this descent). The data we present confirm this model to the point of emergence of serogroup O157 from serotype O55:H7 -------.
In summary, the architecture of the E. coli O157:H7 chromosome is considerably more complex and diversified than previously recognized; its evolution involves either parallel acquisition of stx2 bacteriophages or, more likely, intrabacterial stx2 bacteriophage insertion site changes. Antibiotics promote excisions of complete and truncated bacteriophages.
Previous phylogenetic studies have inferred a stepwise evo-lutionary model that STEC O157 strains descended from an O55:H7-like enteropathogenic ancestor by acquisition of bacteriophage-derived Shiga toxins (Stx1 and/or Stx2), a large virulence plasmid (pO157), and the transition of somatic antigen O55 to O157 (Feng et al. 1998; Reid et al. 2000; Wick et al. 2005). Loss of ability to ferment sorbitol (SOR) and produce _-glucuronidase (GUD) are two key landmarks in the stepwise evolution of STEC O157, which led to emergence of the contemporary GUD_, SOR_ phenotype (Karch et al. 1993; Hayes et al. 1995; Feng et al. 1998; Monday et al. 2001, 2004). However, the time
frame behind the stepwise evolution of STEC O157 remains unknown yet intriguing.
Enterohamorrhagig E. coli (EHEC are associated with gastrointestinal and systemic illness in humans. This illness can range in severity from uncomplicated diarrhea to hemorrhagic colitis and the sometimes fatal hemolytic uremic syndrome. EHEC posses a number of common virulence traits, sucha s the production of one or more types of antigenetically distinct Shiga toxins (Stx1 and Stx2), a .............
E. coli 0157 H7 is the EHEC serotype most often associated with disease outbreaks and with the onset of severe diseace in U.S., Canada, and the UK. ........... O-islands (OI) in Sakai and EDL933 strains......some of teh regions must by responsible for the virulence characteristics that were acquired during evolution of E. coli O157:H7.
E. coli O157:H7 strains are believed to comprise a clonal complex of related genotypes that are found worldwide. It has been suggested that E. coli O157:H7 arose from the enteropathogenic E. coli serotype O55:H7 through sequential acquisition of virulence traits and serotype change [11-13]. A step-wise evolution of E. coli O157:H7 from enteropathogenic E. coli O55:H7 was recently proposed, based on the properties of specific existent strains that carry intermediate characteristics and are presumed to represent intermediates in the evolution of this EHEC serotype [11,13]. The proposed evolutionary pathway includes lysogenization by an stx2-converting phage followed by a shift in serotype from O55 to O157 brought about by acquisition of the O157 gnd-rfb locus . The EHEC large plasmid was then acquired by the organism and the ability to ferment sorbitol was lost. The sorbitol-non-fermenting O157:H7 ancestor was subsequently lysogenized with an stx1-converting phage and, finally, acquired a frameshift mutation in the uidA gene, resulting in loss of β-glucuronidase activity .