Transmission route for 183 (52%) was foodborne, 74 (21%) unknown, 50 (14%) person-to-person, 31 (9%) waterborne, 11 (3%) animal contact, and 1 (0.3%) laboratory-related

The incubation period can range from 3 to 8 days

The antibiotic used depends upon susceptibility patterns in the particular geographical region. Currently, the antibiotics of choice are fluoroquinolones or azithromycin, with an emerging role for rifaximin

Resistance to beta-lactam antibiotics has become a particular problem in recent decades, as strains of bacteria that produce extended-spectrum beta-lactamases have become more common.[55] These beta-lactamase enzymes make many, if not all, of the penicillins and cephalosporins ineffective as therapy

In stool samples, microscopy will show gram-negative rods, with no particular cell arrangement. Then, either MacConkey agar or EMB agar (or both) are inoculated with the stool. On MacConkey agar, deep red colonies are produced, as the organism is lactose-positive, and fermentation of this sugar will cause the medium's pH to drop, leading to darkening of the medium. Growth on EMB agar produces black colonies with a greenish-black metallic sheen. This is diagnostic of E. coli. The organism is also lysine positive, and grows on TSI slant with a (A/A/g+/H2S-) profile. Also, IMViC is {+ + – -} for E. coli; as it is indole-positive (red ring) and methyl red-positive (bright red), but VP-negative (no change-colourless) and citrate-negative (no change-green colour).

E. coli O157:H7 infection often causes severe, acute hemorrhagic diarrhea (although nonhemorrhagic diarrhea is also possible) and abdominal cramps. Usually little or no fever is present, and the illness resolves in five to 10 days. It can also be asymptomatic.

Antibiotics that interfere with DNA synthesis, such as fluoroquinolones, have been shown to induce the Stx-bearing bacteriophage and cause increased production of toxins.

Although Tir is essential for the strong bacterial attachment to host cells, and is a key molecule involved in the attaching and effacing lesion observed during infection, it has since been discovered to suppress innate immune signaling pathways

extracellular pathogens such as members of the Attaching and Effacing (A/E) pathogen group that include enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli O157:H7 (EHEC), and Citrobacter rodentium, inhibit innate immune responses while maintaining intimate contact with the host plasma membrane

A second cardinal virulence factor of E. coli O157:H7 is Shiga toxin, which causes bloody diarrhea and hemolytic uremic syndrome (HUS), a sequelae of EHEC infection. E. coli O157:H7 produces Stx-2, an A-B toxin comprised of a single A subunit noncovalently associated with a pentamer of B subunits. The B subunits bind specifically to globotrioacyl ceramide on host cell cytosolic membranes and facilitates A-subunit uptake by endocytosis. Stx is an N-glycosidase that targets the 28S rRNA, which it depurinates at a specific adenine residue, causing protein synthesis to cease and infected cells to die from apoptosis

Lipid A is the toxic component of LPS, also known as endotoxin, which is a heat-stable toxin

outer facing leaflet of lipopolysaccharide (LPS)

Locus of Enterocyte Effacement (LEE), which is contained on a pathogenicity island that encodes all of the gene products needed for attaching and effacing the colonic epithelium

Sorbitol non-fermenting colonies should be assayed for Shiga toxin using EIA or PCR

cefixime tellurite-sorbitol MacConkey agar (CT-SMAC), or CHROMagar O157

four distinct systems for acid tolerance. There are four corresponding acid resistance (AR) gene systems. The mechanism of AR1 is unknown. AR2, AR3, and AR4 each depend upon amino acid decarboxylation and consequent consumption of protons, whcih results in pH homeostasis. Expression of the AR systems is induced by acid environment, anaerobiosis, entry into stationary phase. Collectively, one or more of these systems is likely to be "on" when EHEC is exposed to acid, as would be expected to occur upon consumption by a potential host and subsequent passage through the stomach

EHEC virulence factors include the ability to adhere tightly to plant materials, acid tolerance, attachment and effacement of intestinal epithelium, and production of endotoxin and Shiga toxin. The regulator of "hyper-adherence", TdcR, and OmpA, an outer membrane protein that is expressed during hyper-adherence are implicated in binding of EHEC to alfalfa sprouts and seed coats. Loss of these virulence factors results in decreased adherence.

E. coli O157:H7 readily colonizes the mammalian large intestine, including humans

Tissue tropism of EHEC at the rectal-anal junction and its stable colonization at this anatomical location ensures its persistence and shedding in feces

Treatment of EHEC typically involves rehydration without administration of antibiotics and hospitalization in severe cases, especially HUS.

E. coli pathotypes that cause diarrhea are transmitted via contaminated food or water, or through contact with infected animals or people

motile by means of peritrichous flagella

facultative anaerobe

Gram negative rod

E. coli (EHEC) typically cause acute bloody diarrhea, which may lead to hemolytic-uremic syndrome. Symptoms are abdominal cramps and diarrhea that may be grossly bloody. Fever is not prominent.

Multistate Outbreak of Shiga toxin-producing Escherichia coli O157:H7 Infections Linked to I.M. Healthy Brand SoyNut Butter (Final Update)

Multistate Outbreak of Shiga toxin-producing Escherichia coli O157:H7 Infections Linked to I.M. Healthy Brand SoyNut Butter (Final Update)

Bovine manure can harbor viable EHEC for more than seven weeks (Wang et al., 1996), and the long-term environmental persistence of EHEC poses an increased risk for transmission of EHEC through the fecal-oral route through wash-off to nearby farms or in contaminated grass consumed by other cattle.

humans acquire EHEC by consuming contaminated bovine-derived products such as meat, milk, and dairy products (Armstrong et al., 1996) or contaminated water, unpasteurized apple drinks, and vegetables (Cody et al., 1999; Hilborn et al., 1999; Olsen et al., 2002). Direct contact with ruminants at petting zoos or through interactions with infected people within families, daycare centers, and healthcare institutes represent another source of EHEC transmission

EHEC colonizes in the colon and causes electrolyte imbalances

Antibiotics promote Shiga toxin production by enhancing the replication and expression of stx genes that are encoded within a chromosomally integrated lambdoid prophage genome. Stx induction also promotes phage-mediated lysis of the EHEC cell envelope, allowing for the release and dissemination of Shiga toxin into the environment

patients treated with antibiotics for EHEC enteritis had a higher risk of developing HUS

Currently no treatment is available for EHEC infections (Goldwater and Bettelheim, 2012). The use of conventional antibiotics exacerbates Shiga toxin-mediated cytotoxicity

life-threatening complication hemolytic uremic syndrome (HUS)

abdominal cramps and bloody diarrhea

Cattle are a natural reservoir of EHEC, and approximately 75% of EHEC outbreaks are linked to the consumption of contaminated bovine-derived products

bloody diarrhea and hemolytic uremic syndrome (HUS)

Cattle are a natural reservoir of EHEC, and approximately 75% of EHEC outbreaks are linked to the consumption of contaminated bovine-derived products

antimicrobials trigger an SOS response in EHEC that promotes the release of the potent Shiga toxin that is responsible for much of the morbidity and mortality associated with EHEC infection

Enterohemorrhagic Escherichia coli (EHEC) serotype O157:H7 is a human pathogen responsible for outbreaks of bloody diarrhea and hemolytic uremic syndrome (HUS) worldwide

Cattle are a major reservoir

In anepidemiology study conducted by the Centers for Disease Controland Prevention, patients treated with antibiotics for EHEC enteri-tis had a higher risk of developing HUS

Currently no treatment is available for EHEC infections

75% of EHEC outbreaks are linked to the consumption of contaminatedbovine-derived products

Plasmid O157 (pO157)

Stxs cross the intestinal barrier and bind to endothelial cells. At this point they presumably injure the host cell by inhibition of protein synthesis, stimulation of prothrombotic messages, or induction of apoptosis.