**3.3 Antibiotic resistance in STEC**

Treatment of STEC infections with antibiotics is not encouraged as this might exacerbate the disease by activating the lytic cycle of the phage carrying Shiga toxin that could aggravate tissue damage in infected individuals. Antibiotics such as rifaximin, fosfomycin, azithromycin, and meropenem that do not encourage the release of Shiga toxin have been used for the treatment of early onset of STEC infection to prevent the progression of the diseases to HUS [90].

Several studies on the prevalence of antibiotic resistance in STEC from different countries and host or environments have reported that resistance to betalactams, sulfonamide, tetracycline, and trimethoprim are common STEC, while multidrug-resistance is more frequent in non-O157 than O157:H7 serotypes [91]. For STEC O157, resistance to ampicillin and cephalothin is common in strains of human origin, whereas tetracycline and sulphamethoxazole resistances are frequent in strains of animal origin [92]. In a study involving 54 STEC strains recovered from cattle and pigs, genetic determinants that encode resistance to trimethoprim (*dfrA1*), tetracycline (*tetA* and *tetB*), beta-lactam (*bla*TEM−1), and aminoglycoside (*aac(6)-Ib*) were found in the great majority (≥81%) of the isolates, while chloramphenicol resistance gene (*cat1*) was also carried in more than 50% of the collection [93]. Likewise, in a 15-year surveillance study of STEC in Sweden [94], 70 antibiotic resistance determinants that were associated with 10 different classes of antibiotics were found in 184 STEC isolates, where 50% of these genes were present in all isolates. Six resistance determinants to fluoroquinolone (*crp*, *hns*, *acrB*, *marA*, *mdtM*, and *emrA*) were found to be frequent. Equally, *emrE* that encodes resistance to multiple antibiotics was associated with STEC O157:H7, whereas *fosA7, sat-1,* and *bla*TEM–150 and *dfrA5* were associated with non-STEC O157 serotype.
