Escherichia coli that are commonly residing in human colon and the strains that cause infections in the gut are called enterohaemorrhagic E. coli (EHEC). Shiga toxin-producing E. coli (STEC), E. coli O157:H7 and E. coli O25:H4 are major human pathogens known to be responsible for infections worldwide (Farfan & Torres, 2012). Moreover, seven E. coli serotypes such as O26, O45, O103, O111, O121, O145 and O157 have been reported as food poisonous bacteria (Singh et al., 2015). Since the introduction of antibiotics, overuse and misuse of those antibiotics have accelerated the anti-bacterial resistance development. This is one of the greatest threats in public health worldwide. As reported, most of the pathogenic strains are resistant to β-lactamases, cephalosporins, tetracycline and fluoroquinolones (Chopra & Roberts, 2001; Diarra et al., 2009; Hornish & Kotarski, 2002). In our previous report, E. coli Sw1 isolated from faeces of piglets having diarrhoea was resistance to ampicillin (93%), penicillin (69%), kanamycin (63%) and tetracycline (46%) at 100 µg ml −1 (Easwaran, Paudel, De Zoysa, & Shin, 2015). Generally, ampicillin could penetrate Gram-positive as well as Gram-negative bacteria and inhibits the bacterial cell wall synthesis, and finally undergoes cell lysis resulting in bacteriolytic activity (Li et al., 2019). Kanamycin interferes the protein synthesis by binding 30S subunit of the bacterial ribosomes, allowing incorrect alignment with the mRNA, thus causing incorrect placing of amino acid into the peptide (Marti et al., 2019). Further, chloramphenicol belongs to class phenicols inhibits the bacterial protein synthesis showing a broad spectrum bacteriostatic activity (Dinos et al., 2016). However, bacterial resistance develops towards antibiotics via either horizontal (exogenous) or vertical (endogenous) evolution. In a single bacterium, it develops