Submitted to: Journal of Food Protection
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 22, 2008
Publication Date: November 6, 2008
Citation: Fratamico, P.M., Bhagwat, A.A., Injaian, L., Cray, P.J. 2008. Characterization of shiga toxin-producing escherichia coli strains isolated from swine feces. Journal of Food Protection. 5(6):827-838. Interpretive Summary: A group of bacteria known as Shiga toxin-producing Escherichia coli (STEC) that produce one or more potent toxins belonging to the Shiga toxin family are important emerging food-borne pathogens. These bacteria are commonly found in animals, including pigs and cattle, and have been associated with food-borne disease outbreaks. Although STEC of different varieties, known as serotypes, are frequently found in food, animals, and the environment, only some serotypes are more commonly associated with human illness. To gain a better understanding of the potential of swine STEC strains to cause human illness, 219 different STEC isolated from pig feces were characterized to determine the presence of specific genes that are found in E. coli that cause disease (virulence genes), their resistance to different antibiotics, and their tolerance to acid environments. The STEC strains consisted of 58 different serotypes having 23 different virulence gene profiles. The strains showed considerable resistance to several antibiotics used in swine production and which are also important in human clinical medicine. It is noteworthy that 95 percent of the STEC strains were resistant to tetracycline, and one strain was resistant to 15 different antibiotics. Furthermore, the STEC were tolerant to different acid conditions, similar to what may be encountered in the human gastrointestinal tract. This study showed that swine STEC comprise a heterogeneous group of organisms, and their tolerance to acid environments and the possession of different combinations of E. coli virulence genes indicate that swine STEC can potentially cause human illness.
Technical Abstract: Shiga toxin-producing E. coli (STEC, 219 strains) isolated from swine feces belonging to different serogroups were characterized to determine their virulence gene and antibiotic resistance profiles, as well as acid tolerance. Twenty-nine out of 219 (13 percent) of the isolates harbored the stx1 gene, 14 (6 percent) stx2, 176 (80 percent) stx2e, 46 (21 percent) estIa, 14 (6.4 percent) estIb, 10 (4.6 percent) fedA, 94 (42.9 percent) astA, 25 (11.4 percent) hly933, and 1 (0.46 percent) cdt-III. None of the strains possessed the elt, bfp, faeG, fanA, fasA, fimF41a, cnf-1, cnf-2, eaeA, cdt-I, or cdt-IV genes. The strains were also tested for antimicrobial susceptibility using 16 antibiotics. The STEC isolates displayed resistance most often to tetracycline (95.4 percent), sulfamethoxazole (53.4 percent), kanamycin (38.4 percent), streptomycin (34.7 percent), and chloramphenicol (22.4 percent). An E. coli serotype O20:H42 strain, which was positive for stx2e and astA, was resistant to all of the antibiotics tested, except for amikacin. In addition, 52 of the swine isolates were examined for their ability to withstand acid challenge by three types of acid resistance (AR) pathways, AR1 (rpoS dependent), AR2 (glutamate dependent) and AR3 (arginine dependent). None of the strains was defective in the AR1 resistance pathway, while one strain was defective in the AR2 pathway under aerobic growth conditions, but was fully functional under anaerobic growth conditions. Eight out of 52 strains were defective in the AR3 pathway. The strain that was defective in AR2 was fully functional in the AR3 pathway. Since acid resistance plays a vital role in the survival and virulence of these strains, differences among the isolates to induce AR pathways may play a significant role in determining their infective dose. This study demonstrates that swine STEC comprise a heterogeneous group of organisms, and the possession of different combinations of E. coli virulence genes indicate that some swine STEC can potentially cause human illness.