Pathogenesis of ETEC involves the establishment of adherence to the epithelium of the small intestine by means of colonization factors (CF) (Oh et al. 2014). This is followed by the production of en- terotoxins (a heat-stable toxin (st) and/or a heat-labile toxin (lt)), which stimulate the lining of the intestine causing secretion of excessive uid, often leading to diar- rhea (CDC 2014). Enterotoxigenic (ETEC) strains are responsible for millions of infections cases worldwide, and it is one of the most important pathogens associated with death following moderate to severe diarrhea in children (Luo et al. 2014). Clinical symptoms of ETEC infection include profuse watery diarrhea with abdominal cramps (usually self-limiting) while fever, headache, nausea, and vomiting are less common symptoms (Yoder et al. 2006). The nondetection of the st gene as observed in our study might have resulted from the loss of the plasmid-encoded gene