Entero-aggregative E.coli (EaggEC).

Entero-aggregative E.coli (EaggEC).
Mathew and Coworkers described afifty reputed group of Enterovirulent E.coli associated with traveler’s diarrhea in Mexico. This new group was associated to more than 40% of HEP-2 cells in tissue culture assays (Janda and Abbott 1998).

Cravioto et al. (1979) observed that EPEC adhere to HEP-2 cells. However, these investigators also showed that many E.coli strains adhere to HEP-2 cells as well and, moreover, that the adherence pattern of EPEC was described as localized adherence (LA), denoting the presence of clusters or microcolonies on the surface of HEP-2 cells. In contrast, non-EPEC did not adhere in the characteristic microcolony morphology, instead displaying a phenotype initially described as (DA) (Nataro et al., 1987a).

The HEP-2 adherence properties of E.coli isolated phenotype can be sub-devided into three categories, (i)Localized (now EPEC), (ii) Aggregative (now EAEC), (iii) Diffuse (now DAEC).

Aggregative adherence (AA) distinguished by prominent, stacked brick autoagglutination of the bacterial cells to each other, which often occurred on the surface of the cells, as well as on the glass coverslip free from the HEP-2 cells.

Diffusely adherent (DA) bacteria were seen dispersed over the surface of the HEP-2 cell, with little aggregation and little adherence to the glass coverslip free from cells (Nataro, 2001).

1.3.12.1. Pathogenesis.
The pathogenicity of EAEC is not thoroughly under stood, however a characteristic histopathological lesion and several candidate virulence factors have been described.; the site of EAEC infection is not known. In an out break of EAEC diarrhea in infants, the illume was shown to be involved (Eslava et al., 1993). The short incubation period of as little as 7 hours, is most consistent with a small bowel site of infection (Nataro et al., 1995a).

Hicks et al. (1996) and Knutton et al. (1992) however shown that EAEC can adhere to small and to an even greater extent to large-bowel section vitro.

EAEC characteristically enhance mucus secretions by the mucosa, with trapping of the bacteria in a bacterium-mucus biofilm (Tzipori et al., 1992), and volenteers fed EAEC develop a diarrhea predominately mucoid in character (Nataro, 2001).

Infection with EAEC has repeatedly been shown to induce cytotoxic effects on the intestinal mucosa. In rabbit and rat ileal loop models (Vial et al., 1988).

EAEC induce a destructive lesion demonstrated by light microscopy. The lesion is characterized by shortening of the villi, hemorrhage necrosis of the villus tips and mild inflammatory response with oedema and mononuclear infiltration of the sub-mucosa (Nataro, 2001).

Thus, diarrheagenic E.coli which adhered to HEP- 2 cells but which were not of EPEC serotypes were termed (enteroadherent E.coli) (Mathewson et al., 1986). The term “enteroadherent” is still frequently used but should now be replaced by the more precise terms enteroaggregative and diffusely adherent (Vial et al., 1988).
EAEC strains are currently defined as E.coli strains that do not secrete entertoxine LT or ST and that adhere to HEP-2 cells in an AA pattern (Nataro et al., 1995a).

1.3.12.2. Cytotoxins.
The toxic effects observed in animal models, human intestinal explains and T84 cells are not accompanied by interalization of the bacteria or by intinate attachment. Therefore, several groups have attempted to identify secreted cytotoxins.

Eslava et al. (1998) have identified 108-Kda cytoxin which elicits destructive lesions in the rat ileal loop. This protein was described by serum from patients infected with EAEC (Baldwin et al., 1992).

1.3.12.3. Epidemiology.
Strains of EAEC belong to very diverse combinations of O and H type, and even within an outbreak of diarrheal disease strains with several different serotypes may be isolated. The diversity of serotypes and pathogenic mechanisms observed suggests that the genes encoding the aggregative phenotype may be accepted readily by pathogenic strains of E.coli causing these bacteria to be considered as EAEC (Green wood et al., 2002).

1.3.12.4. Clinical diagnosis.
The clinical feauters of EAEC are a watery, mucoid secretory diarrheal illness with low-grade fever and little to no vomiting. Beside bloody (Cravioto et al., 1991).

Stiner et al. (1998) have found a large percentage of patients excreting EAEC have detectable fecal lactoferrin and supernormal levels of IL-8 in the stool. This observation suggests that EAEC infection may be accompanied by a suitable form of mucosal inflammation.

1.3.12.5. Detection and diagnosis.
EAEC infection is diagnosed definitively by the isolation of E.coli from the stools of patients and the demonstration of AA pattern in the HEP-2 assay.

1.3.12.5.1. HEP-2 assay.
• HEP-2 cells assay remains the gold standard for detection of EAEC. This test involves allowing strains of E.coli to adhere to cell monolayers in vitro and observing the pattern of adhesion by microscopy. Although tissue culture tests are laborious, the pattern of adhesion remains the key assay for detecting EAEC.
• An aggregative adhesion gene probe has proved useful as a comparatively rapid means of screening strains as a prelude to HEP-2 adhesion test (Nataro and Kaper, 1998 and Green wood et al., 2002).