Shiga furthermore, the highest outbreak of this disease

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Last updated: May 2, 2019

Shigatoxin Escherichia coli (STEC) or Verotoxin producing Escherichia coli (VTEC) O157:H7 is animportant pathogen of diarrhoea, hemorrhagic colitis (HC), and the hemolytic uremicsyndrome (HUS) (Nataro and Kaper, 1998).It commonly take a week to reacquirefrom E. coli O157: H7 caused diarrhea, furthermore, some people sensitiveto E. coli O157: H7 strains could sometimes arise Hemolytic UremicSyndrome (HUS), which possibly lead to dangerous kidney failure and even extendsto death (Sanchez A, Navarro RB,2008).Verotoxin producing Escherichia coli (VTEC) arise as acrucial human pathogens in the last two decades.The hemolytic uremic syndrome(HUS) comes ~15% of culture proven childhood Escherichia coli O157:H7 contagions and takes place ~1 week lateron diarrhea begins (Wong, C.

S., Jelacic, S., Heebib, R.

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L., etal,2000).STECO157:H7 is thought to be the single most significant STEC serotype, thoughnon-O157 VTEC have contributed to both sporadic cases and large incidence (Goldwater,P.N., Bettelheim, K.A.1998).

Several E. coli strains have been known tocause haemorrhagic colitis in humans; furthermore, the highest outbreak of thisdisease were detected in relative to O157:H7 (Scotland SM, Willshaw GA, SmithHR, Rowe B.1990).

Globallynon-O157:H7 STEC were most commonnly causes of HUS reported like in Australia,Germany, and Austria (Phillip, Tarr, I., Carrie, Gordon, V., Wayne, Chandler,L.

, 2005).Escherichia coli O157   is the most common member  of pathogenic E. coli strains known diversely as enterohaemorrhagic,verocytotoxin producing and Shiga-toxin-producing organisms.The ?rst outbreaksinduced by E.

coli O157 took place in Oregon and Michigan, USA, in 1982, when itwas isolated from individuals who arise bloody diarrhea and serious abdominalcramps after eating hamburgers in a restaurant (MMWR Morb Mortal Wkly Rep.1982).TheDiarrheagenic Escherichia coli (DEC) can be classified aspathotypes on the basis of gene-specific sequences.The six known pathotypesinclude Diffusely adherent E. coli (DAEC)  Enteroinvasive E. coli  (EIEC), Enterotoxigenic E.

coli (ETEC),Enteropathogenic E. coli (EPEC), Enteroaggregative E. coli(EAEC), and Enterohemorrhagic E.

coli (EHEC) (Iruka, I.N., et al., 2009).VTEChave twenty-five  serogroups identifiedin this study and included four serogroups (077, 096, 0140, and 0162) notprevious described.Out of twenty-five (25) serogroups, fourteen serotypes(02,04,07,08,09,015,(GI-0,022,026,0110,0113,0126, 0157 and 0168) have beenasoociated with human disease(CH and HUS) (Smith, H.

R., Scotland, S.M.1988).Itis  recently observed that STEC asimportant food-borne pathogens, especially O157, O26, O103, O111, O145, O45,O91, O113, O121 and O128 serogroups (Momtaz, Farzan, Rahimi, SafarpoorDehkordi, & Souod, 2012).Withineach pathotype, E coli strains are further characterized according toantigenic variants including O-antigen (lipopolysaccharide), H-antigen(flagellar) and K-antigen (capsular) types (Riley LW, Remis RS, Helgerson SD,zaet al.1983).

STECexpressing somatic (O) antigen 157 and ?agellar (H) antigen and contain seven(7) serotype most frequently isolated from human beings, and these serotypewith the potent and most bearing etiological affiliation with HUS.Strains whichexpress the lipopolysaccharide (LPS) O-antigen 157 (O157 strains) are usuallyassociated with serious clinical manifestations,including bloody diarrhea,hemorrhagic colitis, and hemolytic uremic syndrome (Tarr, P.I. et al., 1995).Ahighly conserved, non-conjugative F-like plasmid, related to pO157, whichranges in size between 92 kb and 104 kb are mostly bears by EHECO157:H7.Sequence analysis shows a heterogeneous mixture conveys of geneticelements, transposons and prophages, as well as parts of other plasmids which,collectively, are indicative of its splotched evolution.

The complete sequenceof pO157 shows 100 open reading frames; among them, 43 indicate similarities toknown proteins.However, the exact role of pO157 in disease pathogenesis isstill  not well known because publishedstudies have reported contradictory findings (Lim JY, Yoon J, Hovde CJ. 2010).

Thedominant STEC serotype is O157:H7; it is the serotype most commonly involved inlarge outbreaks (Paton, A.W., and Paton, J.

C.1998).Shiga toxins (Stx1 and Stx2) or verotoxins (VT1 and VT2) are two potent phage-encodedcytotoxins of STEC.Stx1 and Stx2 are further classified into severalsubtypes; according to the new categorization suggested by Scheutz et al.(Scheutz, F., Teel, L.

D., and Beutin, L., etal.

, 2012).Stx1 consists of three variants, Stx1a, Stx1c and Stx1d, whereas Stx2 is a diverse group composed of seven distinguishable variants, namely Stx2a,Stx2b, Stx2c, Stx2d, Stx2e, Stx2f and Stx2g.Theproduction of Stx may not be aloneresponsible for pathogenesis of STEC (Farfan, M.J., and Torres, A.G.2012).In addition to toxin production, another virulence-associated factor carried by STEC is a protein called intimin which is responsible for attachment of STEC to the intestinal epithelial cells, causing attaching and effacing (AE) lesions in the intestinal mucosa.

The chromosomal gene eae, called intimin which is component of a pathogenicity island termed the locus for enterocyte effacement (LEE).Enterohaemolysin (Ehly), is a factor that may also affect the virulence of STEC are also  known as enterohaemorrhagic E. coli hemolysis (EHEC-HlyA) , which is encoded by ehxA gene (Goldwater, P.N., Bettelheim, K.A.1995).

E. coli O157:H7 comes out to be the predominant serotype found linked with foodborne infections, E. coli O157:H- isolates may also bear these virulence markers and cause disease in humans (Schmidt,H., Biutin, L.

, Karch, H.1995).Six E.

coli virulence genes were characterized by multiplex PCR including;heat-labile enterotoxin (LT; 30%),heat-stable enterotoxins (STa; 33.3%), two Shiga toxins: (Stx1; 86.67%) and (Stx2; 26.67%) acquired from Shiga toxin producing E. coli (STEC) and two enterotoxigenic E.

coli (ETEC) adhesions(F41; 16.67%) and (F5; 13.3%)  (Emad, A.H., and Hend, M.

El. D., et al., 2016).Thisprocess in which bacteria communicate is known as “quorum sensing” which oftenresults in the synthesis of physical structures with unique characteristicsknown as “biofilms”.A biofilm is a surface association of microbial communitythat is imbedded in a self-produced, extra cellular polymeric matrix.Thesediscoveries make entirely a new field has emerged in basic and appliedmicrobiology called “Quorum Sensing” (QS).Though not newly to the environmentalmicrobiologists, persistent infection due to biofilm formation is sure a new andadditional load to clinicians who treat infections (Sritharan, M., Sritharan,V., et al., 2004).Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is thecausative agent of various outbreaks of bloody diarrhea and hemolytic-uremicsyndrome all around the world.Quorum Sensing has been shown to be a Global Regulatory Mechanism inEnterohemorrhagic Eschericha coli O157:H7 (Sperandio, V., et al .2001).Acidresistance (AR) is the ability of bacteria to protect themselves from extremelylow pH (


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