2.9. insert into those host cells which have


2.9. Mechanism of E. coli Pathogenesis  

the pathogenesis of E. coli O157 which causes disease in humans are concerned
with Stx, a bacteriophage encoded
toxins.The toxins increase the intimin-? mediated adherence and the toxins was observed
to in E. coli O157 which lead to the adherence to intestinal epithelial
cells which increases the surface expression of nucleolin on host epithelial
cells (Robinson, C.M., et al.,2006).While this bacteria colonizes in  cattle intestine, and naturally it is
non-pathogenic and does not produce disease in the host.Various factors may bound
the ability of  E. coli O157 to cause
disease in cattle, i.e host responses against such elements, differences
between animal and human host environments a complicated interaction between
microbial factors unambiguously expressed within the gastrointestinal tract
(GIT) of cattle.Mean while at the recto-anal junction of their gastrointestinal
tract (GIT) these factors may also lead towards the persistence of E. coli O157
in these animals (Naylor, S.W.Roe,
A.J.et al.

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The Stx
receptors were absent in the ruminants so they are not sensitive to the  Stx  (Pruimboom- Brees, I.M.et al. 2000).The distributed of stx
genes in STEC colonizing in the gut in animals were not fully  describe.One of the  hypotheses suggested that the antiviral
activity of STEC and a modulation of immune response by Stx are two factor helps in colonizing (Hoffman, M.A.et al. 2006). Stxs are responsible for the infection of EHEC i.e hemolytic
uramic syndrom (HUS), produce strong toxin that insert into those host cells which
have receptors for these toxin and finally block the protein synthesis of the
human cell by damage it ribosomal ribonucleic acid (RNA) (Endo, Y.et al. 1988).

Shows the mechanism of action of the Shiga toxin producing E.coli (STEC).

(i) In
first step the bacteria is attached with the gb-3 layer (glycotriacarceramide-3)
of the host cell. (ii) The production of the stx1 and stx2

 (iii) Further the Stx is carried to the
Golgi body.

(iv) The
toxin enter into the cell (endocytosis occure).

 (v) The clathrin enveloped vesicle were establishment.

 (vi)The toxin is carried to the Golgi body.

(vii) As
a result vesicle break up occurred, detachment of pentamer B from the toxic subunit
A1. (viii) The process of the A1 portion on the rRNA in the 28S portion, acting
as N-glycosidase, substituting an Adenine moiety.

(ix) The
host cells were inabile to translated ribonuclic acid (RNA).

cell death occur (Vinicius, S.C.et
al. 2017).