Characterization of Shiga Toxigenic Escherichia coli O157 and Non-O157 Isolates from Ruminant Feces in Malaysia.

Asanthi Perera,Narelle Fegan,Charles M Clarke,Gary A Dykes

doi:10.1155/2015/382403

Abstract

Shiga toxigenic Escherichia coli (STEC) O157 and several other serogroups of non-O157 STEC are causative agents of severe disease in humans world-wide. The present study was conducted to characterize STEC O157 and non-O157 serogroups O26, O103, O111, O121, O45, and O145 in ruminants in Malaysia. A total of 136 ruminant feces samples were collected from 6 different farms in Peninsular Malaysia. Immunomagnetic beads were used to isolate E. coli O157 and non-O157 serogroups, while PCR was used for the detection and subtyping of STEC isolates. STEC O157:H7 was isolated from 6 (4%) feces samples and all isolates obtained carried stx 2c, eaeA-γ1, and ehxA. Non-O157 STEC was isolated from 2 (1.5%) feces samples with one isolate carrying stx 1a, stx 2a, stx 2c, and ehxA and the other carrying stx 1a alone. The presence of STEC O157 and non-O157 in a small percentage of ruminants in this study together with their virulence characteristics suggests that they may have limited impact on public health.

Highlights

Shiga toxin producing E. coli (STEC), a serologically diverse group of zoonotic pathogens, have emerged as one of the most virulent groups of bacteria associated with cases of food borne disease in humans [1]
The presence of STEC O157 isolates of lineage II in ruminants in Malaysia from this study suggests that these isolates could have less pathogenic potential in humans
Despite the use of specific and sensitive methods of enrichment and Immunomagnetic separation (IMS) followed in this study to isolate STEC O157 and non-O157, it appears that the presence of both STEC O157 and non-O157 in ruminant feces was low (4% and 1.5%, resp.)

Summary

Introduction

Shiga toxin producing E. coli (STEC), a serologically diverse group of zoonotic pathogens, have emerged as one of the most virulent groups of bacteria associated with cases of food borne disease in humans [1]. Production of Shiga toxin (Stx) is considered as the major virulence factor of STEC [1] which contributes to the development of HUS in humans [2]. Accessory virulence factors include a 34 kb chromosomal pathogenicity island called the “locus for enterocyte effacement” (LEE) carrying several virulence associated genes, such as the attaching and effacing (eaeA) gene, and a large plasmid (60 MDa) with an ehxA gene encoding an enterohemolysin. EaeA encodes an outer-membrane protein called intimin which enables the intimate adherence of STEC to the intestinal epithelium of the host [3]. The enterohemolysin protein is implicated in extracting iron from the blood released into the intestine [4]

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