Nonfimbrial Adhesin Mutants Reveal Divergent Escherichia coli O157:H7 Adherence Mechanisms on Human and Cattle Epithelial Cells.

Matthew R Moreau,Terrance M Arthur,Indira T Kudva,Lingling Li,Rebecca Cote,Vivek Kapur,Robab Katani,Todd R Callaway

doi:10.1155/2021/8868151

Matthew R Moreau, Terrance M Arthur + Show 6 more

Open Access

https://doi.org/10.1155/2021/8868151

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Abstract

Shiga toxin-producing, enterohemorrhagic Escherichia coli (EHEC) serotype O157:H7 is a major foodborne pathogen causing symptoms ranging from simple intestinal discomfort to bloody diarrhea and life-threatening hemolytic uremic syndrome in humans. Cattle can be asymptomatically colonized by O157:H7 predominantly at the rectoanal junction (RAJ). Colonization of the RAJ is highly associated with the shedding of O157:H7 in bovine feces. Supershedding (SS) is a phenomenon that has been reported in some cattle that shed more than 104 colony-forming units of O57:H7 per gram of feces, 100–1000 times more or greater than normal shedders. The unique bovine RAJ cell adherence model revealed that O157:H7 employs a LEE-independent mechanism of attachment to one of the RAJ cell types, the squamous epithelial (RSE) cells. Nine nonfimbrial adhesins were selected to determine their role in the characteristic hyperadherent phenotype of SS O157 on bovine RSE cells, in comparison with human HEp-2 cells. A number of single nucleotide polymorphisms (SNPs) were found amongst these nonfimbrial adhesins across a number of SS isolates. In human cells, deletion of yfaL reduced the adherence of both EDL933 and SS17. However, deletion of eae resulted in a significant loss of adherence in SS17 whereas deletion of wzzB and iha in EDL933 resulted in the same loss of adherence to HEp-2 cells. On RSE cells, none of these nonfimbrial deletion mutants were able to alter the adherence phenotype of SS17. In EDL933, deletion of cah resulted in mitigated adherence. Surprisingly, four nonfimbrial adhesin gene deletions were actually able to confer the hyperadherent phenotype on RSE cells. Overall, this study reveals that the contribution of nonfimbrial adhesins to the adherence mechanisms and functions of O157:H7 is both strain and host cell type dependent as well as indicates a possible role of these nonfimbrial adhesins in the SS phenotype exhibited on RSE cells.

Highlights

Shiga toxin-producing Escherichia coli are the most prevalent of the 6 major pathotypes of E. coli and are responsible for approximately 265,000 infections annually, in the US alone [1, 2].e serotype O157:H7, an enterohemorrhagic E. coli (EHEC), is the cause of 40% of those infections whose clinical symptoms range from watery or bloody stools and abdominal cramps to renal damage and/or failure and potentially life-threatening hemolytic uremic syndrome (HUS) [2,3,4]
Nine nonfimbrial genes involved in adherence were chosen from the criteria shown in Figure 1. e criteria considered for the genes of interest were that the gene and/or gene product must be related to adherence, exhibit a nonsynonymous single-nucleotide polymorphism in SS17 compared to EDL933, and/ or expressed in the proteome array performed by Kudva and colleagues
With asymptomatic cattle being the primary reservoirs of O157:H7, supershedding cattle have the most influence on bacterial burden on the environment [12]. e most efficient way to prevent illness from ever occurring in humans is to prevent the colonization and spread of O157:H7 through its source [41]. e ability to colonize the rectoanal junction (RAJ) is critically linked to the ability of O157:H7 to persist in cattle, and this colonization event seems to be important in influencing changes in O157:H7 shedding, such as supershedding [8, 11]

Summary

Introduction

Shiga toxin-producing Escherichia coli are the most prevalent of the 6 major pathotypes of E. coli and are responsible for approximately 265,000 infections annually, in the US alone [1, 2].e serotype O157:H7, an enterohemorrhagic E. coli (EHEC), is the cause of 40% of those infections whose clinical symptoms range from watery or bloody stools and abdominal cramps to renal damage and/or failure and potentially life-threatening hemolytic uremic syndrome (HUS) [2,3,4]. Shiga toxin-producing Escherichia coli are the most prevalent of the 6 major pathotypes of E. coli and are responsible for approximately 265,000 infections annually, in the US alone [1, 2]. Despite causing disease in the human host, cattle colonized with O157:H7 are asymptomatic [1,2,3]. Cattle are the primary reservoirs and the primary site of colonization for O157:H7 in cattle is the rectoanal junction known as the RAJ [2]. Supershedder (SS) cattle, on the other hand, shed ≥104 CFU/g of O157:H7 [9]. Another study in Scotland showed that 80% of all transmission events to other cattle on farms were caused by SS E. coli [10, 12]

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