Shiga Toxin producing E. coli: A sleeping beast

The risk of increasing cases of infection with Shiga Toxin producing E. coli (STEC) has a direct link with the promotion of consumption of foods like leafy vegetables like lettuce and sprouts and seeds [14]. Moreover, the food items can also get contaminated through contaminated water, soil, fertilizer, air, and through the slaughtering process ^[15].

The largest outbreak of STEC reported so far happened in Japan, in 1996 causing above 7500 cases [16]. An outbreak in china in 1999 was caused by the O157: H7 XuZhou21strain, causing Hemolytic Uremic Syndrome (HUS) in 195 people with a 90% mortality rate and with (85.6%) older than 50. The probable cause was the risky conditions and the nearness to animal carriers [1].

In Germany, in 2011, an ‘Entero-Aggregating E. coli’ (EAEC) hybrid serotype O104:H4 was detected with the Stx2 gene causing 3816 reported cases of infection with 845 patients (22%) presenting HUS and 36 (4.2%) deaths. Infections were related to the consumption of contaminated raw fenugreek by animals [2]. New pathogenic strains of STEC are always possible since many of the serotypes evolved from Entero-pathogenic E. coli (EPEC) [3]. There is great diversity in the group of Shiga-toxin-producing E. coli and understanding the virulence factors, pathogenic mechanism, and animal reservoirs could largely help to develop prevention strategies ^[21].

STEC species are classified into 2 subtypes: O157 and non-O157, with cases involving O157 strains more frequently associated with HUS and thrombotic thrombocytopenic purpura ^[4]. The infectious dose of STEC is considerably low and even just 100 cells are enough to cause infection. The symptoms of STEC infection start to appear after a short incubation time, usually three to four days. The common symptoms are diarrhea, abdominal pain leading mostly to bloody diarrhea ^[17].

The use of antimicrobial agents is not suggested in STEC infection because of high risk of developing HUS. Moreover, the use of growth promoting substances such as antimicrobials may lead to the dissemination of virulence genes to the emergence of new pathogenic strains ^[18].

Many factors are associated with the risk of developing HUS from STEC infection such as demographics, immunity and lifestyles of affectees, virulence factors, toxin type and serotype of E. coli ^[11]. The post HUS complications include chronic renal problems, diabetes mellitus, neurological disorders, colon stenosis, hypertension, urinary abnormalities and bile stones ^[19].

The Shiga toxin comprises of a subunit A and another 5 subunits B. The subunit A is responsible for toxic action by inhibiting protein synthesis whereas subunits B ensure the binding of the toxin to the host cell globotriacylceramide (Gb3) receptor ^[11]. Although the STEC group can elicit innate and adaptive immunity by causing intestinal inflammation and small mucosal hemorrhages ^[12], however, ruminants are asymptomatic to Shiga toxin pathogenicity, may be because they do not possess the glycotriacarceramide-3 layer on the cell surface ^[13].

Tolerance of STEC to extreme temperatures is an important feature of the STEC group, implicated in many outbreaks, making some able to survive under freezing temperatures even for several months ^[5]. The main source of dissemination of the serotypes is supposed to be the super shedding animals, those presenting a high number of pathogens elimination by feces ^[6].

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Despite many doubts concerning the super shedding animals, it is believed that the main cause is the formation of a biofilm in the intestinal epithelium ^[7]. Several official and unofficial methods have been standardized for STEC detection, nevertheless, no gold standard for STEC isolation and cultivation has been developed [8]. There have been developed several methodologies for the detection of such animals in herds [9]. However, there has been a lack of a good standard method for detecting all pathogenic STEC ^[10].

The most effective way to avoid any such outbreaks of STEC is to avoid contamination of food with STEC strains by improving hygiene of food processing chains Moreover, it is necessary to improve detection methods encompassing O157 and nonO157 strains and also the efforts to decrease super shedding animals should be made ^[21].

REFERENCES

1. Xiong Y, Wang P, Lan R, Ye C, Wang H, Ren J, Jing H, Yiting Wang, Zhou Z, Bai X, Cui Z, Luo X, Zhao A, Wang Y, Zhang S, Sun H, Wang L, Xu J. 2012. A novel Escherichia coli O157:H7 clone causing a major hemolytic uremic syndrome outbreak in China. PloS One 7: e36144.
2. Frank C, Werber D, Cramer JP, Askar M, Faber M, an der Heiden M, Bernard H, Fruth A, Prager R, Spode A, Wadl M, Zoufaly A, Jordan S, Kemper MJ, Follin P, M¨uller L, King LA, Rosner B, Buchholz U, Stark K, Krause G. 2011. Epidemic profile of Shiga-toxin-producing Escherichia coli O104:H4 outbreak in Germany. N Engl J Med 365:1771–80.
3. Eichhorn I, Heidemanns K, Semmler T, Kinnemann B, Mellmann A, Harmsen D, Anjum MF, Schmidt H, Fruth A, Valentin-Weigand P, Heesemann J, Suerbaum S, Karch H, Wieler LH. 2015. Highly virulent non-O157 enterohemorrhagic Escherichia coli (EHEC) serotypes reflect similar phylogenetic lineages, providing new insights into the evolution of EHEC. Appl Environ Microbiol 81:7041–7.
4. Oporto B, Esteban JI, Aduriz G, Juste RA, Hurtado A. 2008. Escherichia coli O157:H7 and non-O157 Shiga toxin-producing E. coli in healthy cattle, sheep, and swine herds in northern Spain. Zoon Public Health 55:73–81.
5. De Schrijver K, Buvens G, Poss´e B, Van den Branden D, Oosterlynck O, De Zutter L, Eilers K, Pi´erard D, Dierick K, Van Damme-Lombaerts R, Lauwers C, Jacobs R. 2008. The outbreak of Verocytotoxin-producing E. coli O145 and O26 infections associated with the consumption of ice cream produced at a farm, Belgium, 2007. Euro Surveill Bull Eur Sur Mal Transm Eur Commun Dis Bull 13:8041.
6. Chase-Topping M, Gally D, Low C, Matthews L, Woolhouse M. 2008. Super-shedding and the link between human infection and livestock carriage of Escherichia coli O157. Nat Rev Microbiol 6:904–12.
7. Munns KD, Selinger LB, Stanford K, Guan L, Callaway TR, McAllister TA. 2015. Perspectives on super-shedding of Escherichia coli O157:H7 by cattle. Foodborne Pathog Dis 12:89–103.
8. Conrad CC, Stanford K, McAllister TA, Thomas J, Reuter T. 2016. Competition during enrichment of pathogenic Escherichia coli may result in cultural bias. FACETS 1:114–26.
9. Williams KJ, Ward MP, Dhungyel OP. 2015. A longitudinal study of Escherichia coli O157 shedding and super shedding in dairy heifers. J Food Prot 78:636–42.
10. Smith JL, Fratamico PM, Gunther IVNW. 2014. Shiga toxin-producing Escherichia coli. Adv Appl Microbiol 86:145–97.
11. Karmali MA, Gannon V, Sargeant JM. 2010. Verocytotoxin-producing Escherichia coli (VTEC). Vet Microbiol 140:360–70.
12. Zaheer R, Dugat-Bony E, Holman D, Cousteix E, Xu Y, Munns K, Selinger LJ, Barbieri R, Alexander T, McAllister TA, Selinger LB. 2017. Changes in bacterial community composition of Escherichia coli O157:H7 super-shedder cattle occur in the lower intestine. PloS One 12:e0170050.
13. Bonardi S, Alpigiani I, Tozzoli R, Vismarra A, Zecca V, Greppi C, Bacci C, Bruini I, Brindani F. 2015. Shiga toxin-producing Escherichia coli O157, O26 and O111 in cattle faeces and hides in Italy. Vet Rec Open 2:e000061.
14. Hou Z, Fink RC, Sugawara M, Diez-Gonzalez F, Sadowsky MJ. 2013. Transcriptional and functional responses of Escherichia coli O157:H7 growing in the lettuce rhizoplane. Food Microbiol 35:136–42.
15. Wang Y, Salazar JK. 2016. Culture-independent rapid detection methods for bacterial pathogens and toxins in food matrices. Compr Rev Food Sci Food Saf 15:183–205.
16. Terajima J, Iyoda S, Ohnishi M, Watanabe H. 2014. Shiga toxin (verotoxin)-producing Escherichia coli in Japan. Microbiol Spectr2(5):https://doi.org/10.1128/microbiolspec.EHEC-0011-2013.
17. Nguyen Y, Sperandio V. 2012. Enterohemorrhagic E. coli (EHEC) pathogenesis. Front Cell Infect Microbiol 2:90.
18. K¨ohler B, Karch H, Schmidt H. 2000. Antibacterials that are used as growth promoters in animal husbandry can affect the release of Shiga-toxin-2-converting bacteriophages and Shiga toxin 2 from Escherichia coli strains. Microbiol Read Engl 146:1085–90.
19. Karch H, Tarr PI, Bielaszewska M. 2005. Enterohaemorrhagic Escherichia coli in human medicine. Int J Med Microbiol 295:405–18.
20. Kim J-S, Lee M-S and Kim JH (2020) Recent Updates on Outbreaks of Shiga Toxin-Producing Escherichia coli and Its Potential Reservoirs. Front. Cell. Infect. Microbiol. 10:273. DOI: 10.3389/fcimb.2020.00273
21. Castro, V. S., Carvalho, R. C. T., Conte‐Junior, C. A., & Figuiredo, E. E. S. (2017). Shiga‐toxin producing Escherichia coli: pathogenicity, super shedding, diagnostic methods, occurrence, and foodborne outbreaks. Comprehensive reviews in food science and food safety, 16(6), 1269-1280.