Pathogenic E. Six pathotypes are associated with diarrhea and collectively are referred to as diarrheagenic E. Escherichia coli abbreviated as E. Although most strains of E. Some kinds of E. Still other kinds of E. It does get a bit confusing—even to microbiologists. You might hear these bacteria called verocytotoxic E. The strain of Shiga toxin-producing E. In addition to E.
Other E. First, clinical laboratories must test stool samples for the presence of Shiga toxins. Some types of STEC frequently cause severe disease, including bloody diarrhea and hemolytic uremic syndrome HUS , which is a type of kidney failure. Less is known about the non-O STEC, partly because older laboratory practices did not identify non-O infections. As a whole, the non-O serogroups are less likely to cause severe illness than E.
For example, E. People of any age can become infected. Very young children and the elderly are more likely to develop severe illness and hemolytic uremic syndrome HUS than others, but even healthy older children and young adults can become seriously ill. The symptoms of STEC infections vary for each person but often include severe stomach cramps, diarrhea often bloody , and vomiting. Most people get better within 5—7 days. Some infections are very mild, but others are severe or even life-threatening.
Clues that a person is developing HUS include decreased frequency of urination, feeling very tired, and losing pink color in cheeks and inside the lower eyelids.
Persons with HUS should be hospitalized because their kidneys may stop working and they may develop other serious problems. Most persons with HUS recover within a few weeks, but some suffer permanent damage or die. The symptoms often begin slowly with mild belly pain or non-bloody diarrhea that worsens over several days.
HUS, if it occurs, develops an average 7 days after the first symptoms, when the diarrhea is improving. STEC live in the guts of ruminant animals, including cattle, goats, sheep, deer, and elk. The major source for human illnesses is cattle. STEC that cause human illness generally do not make animals sick.
Contaminated bovine products and crops are predominant sources for human infections. Cattle are the natural reservoir of E. Contaminated ground beef is the most common vehicle for E. Beef products may become contaminated during slaughter, and the process of grinding beef may transfer pathogens from the surface of the meat to the interior.
Therefore, if ground beef is incompletely cooked, the bacteria can survive. In addition, there are a variety of contaminated food vehicles other than ground beef that have been linked to E. The largest outbreak was traced to radish sprout contamination in Osaka, Japan, where 7, individuals were diagnosed with confirmed infections [ 45 ].
Epidemiological studies indicate that these food products seem to have been contaminated through bovine fecal materials. Therefore, prevention of E. To control E. The low pH in the stomach pH 1. The ability to survive in the acidic environment of the stomach increases the chance of bacteria to colonize the intestines and cause infection.
Acid resistance is associated with a lowering of the infectious dose of enteric pathogens [ 60 ]. The low infectious dose is one of the best known characteristics of E.
A variety of studies have reported the AR of E. These studies have determined three efficient AR systems. The first AR system requires the alternative sigma factor RpoS and glucose repression. The rpoS mutant of E. The second AR system requires the addition of arginine during exposure of acidic condition. The arginine decarboxylase adiA and the regulator of adiA cysB were reported in this second AR system. The third AR system requires glutamate for protection at low pH condition.
Whereas only one of the two glutamate decarboxylases is neededfor protection at pH 2. Previous results revealed that glutamate-dependent AR is the most effective protection at pH 2. Moreover, it was shown that alterations in the cell wall membrane or colonic acid production are associated with successful AR.
Thus, E. Three distinct patterns of E. 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. Third, a few rare animals are colonized for a long duration and shed the bacteria from 3 to 12 months or longer. Age, diet, and immunity of individual cattle could also potentially affect bacterial colonization.
Cray and Moon [ 14 ] reported that calves shed E. Reducing the level of carriage of E. The understanding of colonization factors of E. Composting manure is effective in destroying E. Barker et al. Thus, it can be an efficient transmission vehicle of E. To survive in varied environments, E. For example, the exopolysaccharide EPS production of E. These environmental adaptations of E. In addition, the ability to survive outside the host reservoir increases the risk that the pathogen may contaminate crops and produce via bovine manure contamination, irrigation with contaminated water, or direct contact with infected animals [ 42 ].
Defining the virulence factors and mechanisms of E. The production of Stxs is considered essential but not solely responsible for disease. In addition, E. Each of these aspects is described below. Stx is a potent cytotoxin and is bacteriophage-encoded.
Stx is expanded from a single transcriptional unit and causes damage to a variety of cell types [ 29 ]. Stx1 is identical to Stx from Shigella dysenteriae I, but for a single amino acid difference. Virulent isolates of E. Stx2 is known to be more toxic and is more often associated with HC or HUS in human infections than are Stx1 strains [ 6 , 50 ]. Stx has a conserved structure consisting of one enzymatically active A subunit A1 and five identical receptor-binding B subunits B5.
The B5 subunit binds to the specific host receptors globotriaosylceramide Gb3 or globotetraosylceramide Gb4 [ 47 ]. After binding of Stx A1B5 to the host cell, the A subunit is internalized to the cytoplasm. Al inhibits protein synthesis by the specific removal of a single adenine residue from the 28S rRNA of the 60S ribosomal subunit [ 59 ].
The detailed mechanisms of Stx translocation to various tissues are not fully understood. Attached bacteria stimulate host cell actin polymerization accumulation, resulting in a raised attachment pedestal [ 11 ]. The LEE of E. The role of this additional sequence is not clearly defined.
Recently, non-LEE encoded effectors have also been identified, and the elucidation of their roles will further increase the understanding of the pathological phenomena in E.
Plasmids are mobile elements that provide various host beneficial traits, such as resistance to antibiotics and heavy metals, production of toxins and other virulence factors, biotransformations of hydrocarbons, and symbiotic nitrogen fixation [ 22 ].
Plasmid-encoded genes are required for full pathogenesis in many enteropathogenic bacteria including Shigella , Yersinia , Salmonella , and E. The pO is a nonconjugative F-like plasmid with a range size from 92 to kb. The complete sequence of pO in two different outbreak isolates has been published [ 10 , 41 ].
The pO shows a dynamic structure and includes different mobile genetic elements such as transposons, prophages, insertion sequences IS , and parts of other plasmids.
The heterogeneous composition of pO can delimit the co-responses to functional regions of pO Among them, IS or remnants of IS are frequently associated with the virulence-related segments, which are similar to compositions of the large virulence plasmid in Shigella spp.
These results indicate that the actual pO is formed by integration of fragments from evolutionally different species origins into an F-like plasmid, and thus virulence factors or putative virulence factors on the different segments of pO may be from different origins. The complete sequence of pO reveals open reading frames ORFs [ 10 ].
Among them, 43 ORFs showed sufficient similarities to known proteins, suggesting functions, and 22 ORFs had no convincing similarity with any known proteins.
Thirty-five proteins are presumably involved in the pathogenesis of E. However, the biological significance of pO in pathogenesis is not fully understood. Hemolysin was the first described virulence factor of pO [ 4 , 61 ]. Several studies showed that hemolysin is highly conserved among different serotypes of EHEC such as OH7, OH8, and O8:H19, but it is not known if these have identical biological activities [ 7 ]. A gene for a catalase-peroxidase activity katP was identified from pO [ 9 ].
This gene is 2. The KatP enzyme activity of E. The N-terminal signal sequence suggests that this enzyme is transported through the cytoplasmic membrane. The katP gene was found in all E. This enzyme may help E. These genes are located adjacent to the hemolysin locus. An ISlike insertion element was found to be located far from the etp and ehx genes. Similar to the katP gene, etp genes were also found in all E. This T2SS is similar to the pullulanase secretion pathway pulO of Klebsiella oxytoca , but its function has not been identified.
EspP is the pOencoded type V secreted serine protease and is known to cleave pepsin A and human coagulation factor V [ 8 ]. Recently, Dziva et al. Moreover, degradation of human coagulation factor V via EspP could contribute to the mucosal hemorrhage observed in HC patients.
A metalloprotease, StcE, is encoded on pO and specifically cleaves the C1 esterase inhibitor [ 37 ]. The C1 esterase inhibitor is a host regulator of multiple proteolytic cascades related to inflammation pathways, such as the classical complement, intrinsic coagulation, and contact activation. Grys et al. The stcE gene was found all in E. The toxB gene is encoded on a sequence 9. Recent studies showed that ToxB contributes to the adherence of E. However, a mutation of the toxB and efa-1 genes did not influence intestinal colonization in calves or sheep [ 66 ].
Recently, we reported that pO encoded the ecf operon ecf1 — 4 that is temperature regulated by an intrinsically curved DNA [ 76 ]. The double mutant carrying deletions in the ecf4 and its chromosomal copy lpxM of E. However, a single mutant of ecf4 did not show significant difference compared with wild-type E. After the first report that pO was required for the expression of fimbriae and adhesion to epithelial cells, several studies reported conflicting results on the role of pO in adherence to epithelial cells Table 1 [ 74 ].
In vivo studies of pO, using animal models including the mouse, rabbit, and gnobiotic piglet, also showed conflicting results. However, the in vivo studies have limitations because there is no suitable animal model reproducing all aspects of the disease.
Therefore, the precise role of pO in the pathogenesis of E. Recently, we showed that the pO affects the efficiency of E. Consumers should always practice safe food handling and preparation measures, which include the following:. If there is an E. If you cannot determine the source of your food, do not sell or serve it.
Retailers, restaurants, and other food service operators should always take steps to avoid the cross contamination of cutting surfaces and utensils through contact with potentially contaminated products. To report a complaint or adverse event illness or serious allergic reaction , you can. Visit www. Submit Questions Electronically. Get E-mail Updates. Follow Us on Twitter. Outbreak of Foodborne Illness.
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