Wednesday, March 14, 2012

Enteropathogenic E.coli (EPEC).

Enteropathogenic E.coli (EPEC).
The Enteropathogenic E.coli organisms are the oldest known group of coliforms recognized to cause diarrheal disease in humans and has been linked to infant diarrhea in developing world. Once defined solely on the basis of O and H serotypes, EPEC is now defined on the basis of pathogenic charcteristics. Disease is rare in older children and adults, presumably, because of specific O serogroups have been associated with out breaks of EPEC diarrhea (Lewis, 1997). Pathogenesis.
The ability of EPEC strains to cause diarrhea has been confirmed by oral administration of the organisms to babies and incompletely under stool.

Colonilization of the upper part of the small intestine occurs in infantile entiritis associated with EPEC. In many patients, EPEC are seen by electron microscopy to be intimately associated with the mucosal surface and to be partially surrounded by cup like projections (pedestals” of the enterocyte surface and in areas of EPEC attachment the brush border microocilli are lost. Many strains are strongly adhesive to border microvill are lost. Many strains are strongly adhesive to intestinal epithelial cells, and this represents an important pathogenic mechanism. Such strains of E.coli have been termed attaching, effacing E.coli or entero adherent E.coli (EAEC) (Green Wood et al., 2002). Epidemiology. Age distribution:
The most notable feature of the epidemiology of disease due to EPEC is the striking age distribution seen in persons infected with this pathogen. EPEC infection is primarily a disease of infants younger than 2 years. As reviewed by Levine and Edelman (Edelman and Levine 1983). Numerous case-control studies in many countries have shown a strong correlation of isolation of EPEC from infants with diarrhea compared to healthy infants. The correlation is strongest with infants younger than 6 months. In children older than 2 years, EPEC can be isolated from healthy and sick individuals, but a statistically significant correlation with disease is usually not found (Nataro and Kaper 1998). Transmission and reservoirs:
As with other diarrheagenic E.coli strains, transmission of EPEC is fecal-oral, with contaminated hands, contaminated weaning foods, or contaminated fomites serving as vehicles.

Unless strict decontamination procedures are followed, admission of an infant to a pediatric ward can result in contamination of crib lien, toys, hand towels, scales.

The reservoir of EPEC infection is thought to be symptomatic or asymptomatic children and asymptomatic adults carriers, including mothers and persons who handle infants. Numerous studies have documented the spread of infection through hospitals, nurseries (Bower et al., 1989). EPCE in developing countries:
EPEC is a major cause of infants diarrhea in developing countries. Numerous studies have been founds EPEC to be more frequently isolated from infants with diarrhea than from matched healthy controls (Donnenberg 1995). Particulary in the 0 to 6 months age group, EPEC strains are often the most frequently isolated bacterial diarrheal pathogens (Cravioto et al., 1988).

Several studies have shown that breast feeding is protective against diarrhea due to EPEC. Both human colostrum and milk strongly inhibit the adhesion of EPEC to HEP 2 cells in vitro (Camara et al., 1994). Clinical considerations.
EPEC cause primarily acute diarrhea and it was associated with many common symptoms such as watery diarrhea, vomiting and low-grade fever are common symptoms beside malaise (Cohen and Gianella, 1991).

Fecal leukocytes are seen only occasionally, but more sensetive tests for inflammatory diarrhea such as an anti-lactoferrin latex bead agglutination test are frequently positive with EPEC infection.

As with other diarrheal pathogens, the primary goal of treatment of EPEC diarrhea is to prevent dehydration by correcting fluid and electrolyte imblances. Oral rehydration may be sufficient for milder cases, but more severe cases require parenteral rehydration. Correction nutritional imbalance with lactose free formula or breast milk may be insufficient for some severely ill patients, and total parenteral nutrition may be required. A variety of antibiotics have been used to treat EPEC and have proved useful in many cases. There are no vaccines currently available or in clinical trails to prevent disease due to EPEC (Camara et al., 1994). Detection and diagnosis.
The definition of EPEC has changed in recent years as our knowledge of this pathogen has grown. For many years these organisms were defined only by O serogroups, which were subsequently defined to O:H serotypes. This definition changed as additional serotypes were associated with infantile diarrhea (Edelman and Levine 1983).

Citing recent pathogensis data, the second international symposium on EPEC in 1995 reached a consensus on the basic characteristics of EPEC, the most important of these were the A/E histopathology and the absence of Shiga-toxin. Many EHEC strains also produce the A/E lesion, therefore, determining the presence (indicative of EHEC) or absence (indicative of EPEC) of Stx is essential. The sole defining micorbiological characteristic of EPEC, is no longer deemed an essential characteristic of EPEC, although the majority of EPEC strains fall into certain well-recognized O:H serotypes (Green Wood et al., 2002).

There is some debate whether EPEC strains the lack the EAF plasmid are true pathogen or not so it was found that, only EAF-positive strains and not EAF-negative strains were significantly associated with diarrhea (Echeverria et al., 1991).

Furthermore, EAF-negative strains isolated during the course of an epidemiological study could also be derivatives of EHEC that have lost the phasges that encode Stx.

So EPEC: A/E, Stx-negative strains possessing the EAF plasmid would be called “typical EPEC”, while strains doesn’t possess the EAF plasmid would be called “atypical EPEC” (Nataro and Kaper 1998). Diagnostic tests.
Given that EPEC strains, as with other diarrheagenic E.coli strains, are defined on the basis of virulence properties, there are two approaches to the detection of EPEC in the laboratory (i) phenotypic (ii) genotypic. The phenotypic approach requires the use of cell cultures and fluorescence microscopy, and the genotypic method requires the use of DNA hyberdization or PCR (Nataro and Kaper 1998).

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