Abstract

Cattle are the main reservoirs of Shiga toxin producing Escherichia coli (STEC), a major foodborne pathogen associated with acute enteric disease and hemolytic–uremic syndrome in humans. A total of 397 beef and dairy cattle from 5 farms were included in this study, of which 660 samples were collected for 16S rRNA gene sequencing. The microbiota of farms with a high-STEC prevalence (HSP) had greater richness compared to those of farms with a low-STEC prevalence (LSP). Longitudinal analyses showed STEC-shedders from LSP farms had higher microbiome diversity; meanwhile, changes in the microbiome composition in HSP farms were independent of the STEC shedding status. Most of the bacterial genera associated with STEC shedding in dairy farms were also correlated with differences in the percentage of forage in diet and risk factors of STEC carriage such as days in milk, number of lactations, and warm temperatures. Identifying factors that alter the gut microbiota and enable STEC colonization in livestock could lead to novel strategies to prevent fecal shedding and the subsequent transmission to humans.

Highlights

  • Shiga toxin producing Escherichia coli (STEC) is a foodborne pathogen causing 2.8 million cases of acute enteric disease and 230 deaths annually [1]

  • STEC infections are associated with the consumption of contaminated food and water or result from direct contact with cattle feces since cattle represent an important reservoir for this pathogen [2]

  • The low-STEC prevalence (LSP) farms fed animals a lower percentage of forage in their diet (15–65%) and used anthelmintics, while high-STEC prevalence (HSP) farms used a diet almost exclusively based on forage (80–100%) and did not provide anthelmintic treatments

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Summary

Introduction

Shiga toxin producing Escherichia coli (STEC) is a foodborne pathogen causing 2.8 million cases of acute enteric disease and 230 deaths annually [1]. STEC virulence is caused by bacteriophage-encoded Shiga toxins Cattle are more tolerant to STEC due to the lack of Stx receptors (glycolipid globotriaosylceramide, Gb3) in the intestinal tract as well as a lower receptivity of Gb3 receptors present in the kidney and brain [7]. Some STEC strains, classified as enterohemorrhagic E. coli (EHEC), possess the locus of enterocyte effacement (LEE) pathogenicity island that encodes for a type III secretion system and effectors, such as the intimin protein (eae), which are responsible for attaching and effacing (AE) lesion formation [8].

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