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Wednesday, March 14, 2012

Entero-invasive E.coli (EIEC).

Entero-invasive E.coli (EIEC).
Enteroinvasive strains of E.coli (EIEC) are strains produce dysentry with direct penetration, invasion, and destruction of the intestinal mucosa. This diarrheal illnesses is very similar to that produced by Shigella. The EIEC infections seem to occur in adults and children alike (Mahon and Manuselis 2000).

EIEC strains are generally lysine decarboxylase negative, non motile, and lactose negative (Brenner et al., 1973). EIEC apparently lack fimbial adhesions but do not possess a specific adhesions that as in Shigella, is thought to be an outer membrane protein. Also, like Shigella, EIEC are invasive organisms. They do not produce LT or ST and, unlike Shigella, they do not produce the Shiga-toxin (Hale et al., 1997).

1.3.11.1. Pathogenesis.
The pathogenesity is resemble to Shigella pathogenesis. Both organisms have shown to invade the colonic epithilium, a phenotype mediated by both plasmid and chromosomal loci. In addition, both EIEC and Shigella Spp elaborate one or more secretory enterotoxins that may play roles in diarrheal pathogenesis (Nataro, 2001).

1.3.11.2. Invasiveness.
The current model of Shigella and EIEC pathogenesis comprises (i) Epithelial cell penetration, (ii) Lysis, of the endocytic vacuole, (iii) intracellualr multiplication, (iv) directional movement through the cytoplasm, and (v) extension into adjacent epithelial cells (Nataro, 2001).

EIEC and Shigella both cause disease by invading intestinal epithelial. Infection is by ingestion, only a small number of bacteria need to be swallowed as they are relatively resistant to gastiric acid and bile and pass readily into the large intestine where they multiply in the gut lumen. The bacteria passes through the overlying mucus layer, attach to the intestinal epithelial cells and are carried into the cell by endocytosis into the endocytic vacuole which then lysis.

The ability to cause the vacuole to lyse is an important virulence attribute, as organisms unable to do this can’t spread to neighbouring cells. After lysis of the vacuole the bacteria multiply within the epithelial cell and kill it. Spread to neighbouring cells leads to tissue destruction and inflammation which cause dysentry. Pathogenicity in Shigellae and EIEC depends on chromosomal and plasmid genes (Green Wood et al., 2002).

1.3.11.3. Epidemiology.
Epidemiology and ecology of EIEC have been poorly studied. Documented EIEC out breaks are usually foodborne or water borne, although person to person transimission does occur. Infections are usually foodborne but there is also evidence of cross infection. The most common serogroup is O124 (Green Wood et al., 2002).

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