Enterohemorrhagic Escherichia coli O157:H7 is a major foodborne pathogen causing severe disease in humans worldwide. Healthy cattle are a reservoir of E. coli O157:H7, and bovine food products and fresh produce contaminated with bovine waste are the most common sources for disease outbreaks in the United States. E. coli O157:H7 also survives well in the environment. The abilities to cause human disease, colonize the bovine gastrointestinal tract, and survive in the environment require that E. coli O157:H7 adapt to a wide variety of conditions. Three major virulence factors of E. coli O157:H7 have been identified including Shiga toxins, products of the pathogenicity island called the locus of enterocyte effacement, and products of the F-like plasmid pO157. Among these virulence factors, the role of pO157 is least understood. This review provides a board overview of E. coli O157:H7 with an emphasis on pO157.

The human pathogen Escherichia coli O157:H7 causes hemorrhagic colitis and life-threatening sequelae and transiently colonizes healthy cattle at the terminal rectal mucosa. This study analyzed virulence factors important for the clinical manifestations of human E. coli O157:H7 infection for their contribution to the persistence of E. coli in cattle. The colonizing ability of E. coli O157:H7 was compared with those of nonpathogenic E. coli K-12 and isogenic deletion mutants missing Shiga toxin (Stx), the adhesin intimin, its receptor Tir, hemolysin, or the ϳ92-kb pO157. Fully ruminant steers received a single rectal application of one E. coli strain so that effects of mucosal attachment and survival at the terminal rectum could be measured without the impact of bacterial passage through the entire gastrointestinal tract. Colonization was monitored by sensitive recto-anal junction mucosal swab culture. Nonpathogenic E. coli K-12 did not colonize as well as E. coli O157:H7 at the bovine terminal rectal mucosa. The E. coli O157:H7 best able to persist had intimin, Tir, and the pO157. Strains missing even one of these factors were recovered in lower numbers and were cleared faster than the wild type. In contrast, E. coli O157:H7 strains that were missing Stx or hemolysin colonized like the wild type. For these three strains, the number of bacteria increased between days 1 and 4 postapplication and then decreased slowly. In contrast, the numbers of noncolonizing strains (K-12, ⌬tir, and ⌬eae) decreased from the day of application. These patterns consistently predicted long-term colonization or clearance of the bacteria from the bovine terminal rectal mucosa.Enterohemorrhagic Escherichia coli (EHEC) strains are a subset of Shiga toxin-producing E. coli (STEC) that can cause human disease and are threats to public health worldwide (46,49). Human illnesses caused by EHEC range from self-limiting watery diarrhea or hemorrhagic colitis to life-threatening sequelae, the hemolytic-uremic syndrome or thrombotic thrombocytopenic purpura. The predominant EHEC serotype associated with the most severe disease in North America, the United Kingdom, and Japan is O157:H7 (23,42,44,46,59).Cattle are considered the primary reservoir for E. coli O157:H7 and the most common source for food-borne and direct animal contact infections (5, 25, 69). Healthy cattle carry E. coli O157:H7 transiently without suffering pathological symptoms (2,4,26). Individual animals can passively shed E. coli O157:H7 in their feces for a short time (a few days) without establishing a colonized state or can pass fecal E. coli O157:H7 for a longer time (a month or more) if the bacteria colonize and persist (22). The conditions that lead to these different host-bacterium interactions are not understood.It is well accepted that reducing the carriage or prevalence of E. coli O157:H7 in cattle would reduce the risk of human exposure to this pathogen (61). Recently, the recto-anal junction (RAJ) mucosa was identified as the primary site of E. coli O157:H7 colonizatio...

Long-duration consistently Escherichia coli O157:H7 culture-positive cattle were euthanized and necropsied. Tissue and digesta from along the gastrointestinal tract (GIT) were cultured for the bacteria and examined histologically for lymphoid character. E. coli O157:H7 was detected only at the rectoanal junction mucosa and not at any other GIT location.Escherichia coli O157:H7 causes hemorrhagic colitis and the life-threatening sequela hemolytic-uremic syndrome in humans (6). Healthy cattle are the major reservoir for E. coli O157:H7, and contaminated ground beef, direct animal contact, and bovine manure contamination of other foods or water account for the majority of human infections (2, 3). The predominant colonization site of this microorganism in the bovine gastrointestinal tract (GIT) has been identified as the rectoanal junction (RAJ) mucosa (7). Localization to this site is in contrast with other E. coli serotypes that are present in consistent numbers throughout the large intestine without an increase at the RAJ mucosa. This tissue area comprises a clear junction between the stratified squamous epithelium of the anal canal and the columnar epithelial mucosa of the rectum and is a lymphoid follicle-dense mucosa. Although the mechanisms underlying the tropism of this serotype for this lymphoid follicle-rich site are not known, many studies of experimentally and naturally colonized cattle conclude that the RAJ mucosa plays an important role in E. coli O157:H7 bovine carriage of this human pathogen (5,7,8,10,11). Also, application of E. coli O157:H7 at the RAJ mucosa results in carriage of the bacteria similar to that by naturally infected animals (10).Three distinct patterns of E. coli O157:H7 carriage in cattle have been described previously (1, 9, 12). First, animals can be transiently culture positive for short durations of a few days and are considered passive shedders and are likely not colonized at the RAJ mucosa; second, cattle can be colonized and shed the bacteria for an average of 1 month and typically not longer than 2 months; and third, a few rare animals are colonized for a long duration and shed the bacteria from 3 to 12 months or longer. This unique situation in which a few animals develop long-duration colonization (Ͼ2 months) with E. coli O157 is likely due to bacterial association at the RAJ mucosa; however, it may be due to unique colonization by the bacteria at a site(s) in addition to the RAJ mucosa. For example, the gall bladder can harbor Salmonella spp. in carrier animals and a recent investigation reports E. coli O157:H7 in the gall bladders of some cattle at slaughter; however, this report does not provide information about the E. coli O157:H7 culture history of the animals tested, so the duration for which each animal was culture positive is unknown (4). For the first time, the current study investigated the colonization site of E. coli O157:H7 along the GIT of animals for which a documented history of long-duration carriage of E. coli O157:H7 was available. To identify animals t...

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Bacterial biofilms are complex multicellular assemblies, characterized by a heterogeneous extracellular polymeric matrix, that have emerged as hallmarks of persistent infectious diseases. New approaches and quantitative data are needed to elucidate the composition and architecture of biofilms, and such data need to be correlated with mechanical and physicochemical properties that relate to function. We performed a panel of interfacial rheological measurements during biofilm formation at the air-liquid interface by the Escherichia coli strain UTI89, which is noted for its importance in studies of urinary tract infection and for its assembly of functional amyloid fibers termed curli. Brewster-angle microscopy and measurements of the surface elasticity (G(s)') and stress-strain response provided sensitive and quantitative parameters that revealed distinct stages during bacterial colonization, aggregation, and eventual formation of a pellicle at the air-liquid interface. Pellicles that formed under conditions that upregulate curli production exhibited an increase in strength and viscoelastic properties as well as a greater ability to recover from stress-strain perturbation. The results suggest that curli, as hydrophobic extracellular amyloid fibers, enhance the strength, viscoelasticity, and resistance to strain of E. coli biofilms formed at the air-liquid interface.