2.9. Mechanism of E. coli Pathogenesis Inthe pathogenesis of E. coli O157 which causes disease in humans are concernedwith Stx, a bacteriophage encodedtoxins.
The toxins increase the intimin-? mediated adherence and the toxins was observedto in E. coli O157 which lead to the adherence to intestinal epithelialcells which increases the surface expression of nucleolin on host epithelialcells (Robinson, C.M., et al.,2006).
While this bacteria colonizes in cattle intestine, and naturally it isnon-pathogenic and does not produce disease in the host.Various factors may boundthe ability of E. coli O157 to causedisease in cattle, i.
e host responses against such elements, differencesbetween animal and human host environments a complicated interaction betweenmicrobial factors unambiguously expressed within the gastrointestinal tract(GIT) of cattle.Mean while at the recto-anal junction of their gastrointestinaltract (GIT) these factors may also lead towards the persistence of E. coli O157in these animals (Naylor, S.W.
The Stxreceptors were absent in the ruminants so they are not sensitive to the Stx (Pruimboom- Brees, I.M.et al.
2000).The distributed of stxgenes in STEC colonizing in the gut in animals were not fully describe.One of the hypotheses suggested that the antiviralactivity 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 hemolyticuramic syndrom (HUS), produce strong toxin that insert into those host cells whichhave receptors for these toxin and finally block the protein synthesis of thehuman cell by damage it ribosomal ribonucleic acid (RNA) (Endo, Y.
et al. 1988). Figure.03.Shows the mechanism of action of the Shiga toxin producing E.coli (STEC).
(i) Infirst step the bacteria is attached with the gb-3 layer (glycotriacarceramide-3)of the host cell. (ii) The production of the stx1 and stx2occurred. (iii) Further the Stx is carried to theGolgi body.
(iv) Thetoxin enter into the cell (endocytosis occure). (v) The clathrin enveloped vesicle were establishment. (vi)The toxin is carried to the Golgi body. (vii) Asa result vesicle break up occurred, detachment of pentamer B from the toxic subunitA1.
(viii) The process of the A1 portion on the rRNA in the 28S portion, actingas N-glycosidase, substituting an Adenine moiety. (ix) Thehost cells were inabile to translated ribonuclic acid (RNA). (x)Finallycell death occur (Vinicius, S.C.