ETEC is defined as the E.coli strains that elaborate at least one member of two defined groups of enterotoxins: a heat liable toxin (HLT) and aheat stable toxins(HST). The first is a heat-labile enterotoxin (LT) that shows approximately 80% protein sequence identify with the heat-labile cytotoxinic cholera toxin of vibrio cholerae. The second toxin produced by ETEC is a heat-stable with a molecular mass of about 2Kda. Previous studies suggested that ETEC strains carrying both toxins (HLT+ and HST+) predominate clinically followed in decreasing frequency by strains carrying HSt+ only and those carrying HLT+ only. However, a 1996 review of 700ETEC strains collected over a period of more than 30 years found that the relative prevalence of these toxine type I is not different and that individual toxin-producing patterns may be related to serogroup specificity (Sears and Kaper, 1996 and
Tamura et al., 1996).
1.3.9.1. Epidemiology.
ETEC strains are associated with two major clinical syndromes: weaning diarrhea among children in the developing world, and traveler’s diarrhea. The epidemiologic pattern of ETEC disease is determined in large part by a number of factors: (I) Mucosal immunity to ETEC infection develops in exposed individuals, (ii) Even immune asymptomatic individuals may shed large numbers of virulent ETEC organisms in the stool, and (iii) The infection requires a relatively high infectious dose (Nataro and Kaper 1998). These three feautures create a situation in which ETEC contamination of the environment in areas of endemic infections is extremely prevalent, and most infants in such areas will encounter in warm-climate countries are not well under stool, but it seems likely that water contaminated by human (or) animal sewage plays an important part in the spread of infection (Green Wood, 2002).
1.3.9.2. Clinical symptoms.
The most common symptoms associated with ETEC infection are diarrehea (91-97%) and abdominal cramps (80-94%). Stools are typically watery in consistency, often yellow-tinged, and without the presence of mucus, pus or fecal leukocytes (Cohen and Gianella, 1991).
The gastroentritis induced by ETEC infection is typically indicating guishable from secretory diarrheas elicited by other gram-negative enteropathogens. Less often nausea (39-70%), headaches (35-57%), myalgia (50%), weakness (35%). Chills (31%), and low grade fevers (13-22%) are observed (Role et al., 1995).
Vomiting (2-1%) is not commonly associated with ETEC infection, a fact that helps distinguish this illness from gastrointestinal disturbances caused by norwalk virus.
ETEC infections commonly occur in four settings. In less developed countries, ETEC infection predominate in children younger than a years of age. Unlike the relatively mild infections, ETEC gastroentritis in young children in underdeveloped nations can be serve at times, with dehydration and adverse nutritional consequences leading to retardation of normal growth development (Cohen and Gianella, 1991).
Dehydration has also been noted as a consequence of ETEC infection in industrialized countries. As children mature, the incidence of ETEC disease apparently declines, suggesting that immunity may develop in local inhabitants with advancing age (Black et al., 1981).
1.3.9.3. Detection and Diagnosis.
Detection of ETEC has long relied on detection of the enterotoxins (HLT or HST). HST was initially detected in a rabbit ligaled ileal loop assay, but the expense and lack of standarization caused this test to be replaced by the sucking-mouse assay which become the standard test for the presence of HST for many years (Cryan 1990).
The traditional bioassay for detection of HLT involves the use of cell culture, either the Y, adrenal cell assay (or) the chinese hamster ovary (CHO) cell assay (Donta et al., 1974).
DNA probes were found to be useful in the detection of HLT and HST encoding genes in stool and environmental samples. Since that time several advances in ETEC detection have been made, but genetic techniques continue to attract the most detection and use. It should be stressed that there is no perfect test for ETEC decection of colonization factors because of their great number and heterogeneity (Abdul et al., 1994).
Several PCR assays for ETEC are quite sensitive and specific when used directly on clinical samples or on isolated bacterial colonies. A useful adaptation of PCR is the “multiplex” PCR assay in which several PCR primers are combined with the aim of detecting one of several different diarrheagenic E.coli pathotypes in a single reaction (duToit et al., 1993).
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