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|Escherichia coli O157:H7|
|Classification and external resources|
|Escherichia coli O157:H7|
|Classification and external resources|
Transmission is via the fecal-oral route, and most illness has been through undercooked, contaminated ground beef or ground pork being eaten. Importance Enterohemorrhagic Escherichia coli (EHEC) is a subset of pathogenic E. coli that can cause diarrhea or hemorrhagic colitis in humans. Hemorrhagic colitis occasionally progresses to hemolytic uremic syndrome (HUS), an important cause of acute renal failure in children and morbidity and mortality in adults. In the elderly, the case fatality rate for HUS can be as high as 50%. E. coli O157:H7 (EHEC O157:H7) has been recognized as a cause of this syndrome since the 1980s. The reservoirs for EHEC O157:H7 are ruminants, particularly cattle and sheep, which are infected asymptomatically and shed the organism in feces. Other animals such as rabbits and pigs can also carry this organism. Humans acquire EHEC O157:H7 by direct contact with animal carriers, their feces, and contaminated soil or water, or via the ingestion of underdone ground beef, other animal products, and contaminated vegetables and fruit. The infectious dose is very low, which increases the risk of disease. Infections with EHEC in other serogroups, including members of O26, O91, O103, O104, O111, O113, O117, O118, O121, O128 and O145, are increasingly recognized as causes of hemorrhagic colitis and HUS. Some of these organisms may be as significant in human disease as EHEC O157:H7; however, they are not recognized on the media used to isolate this organism, and many laboratories do not routinely screen for other strains. Although many EHEC seem to be carried asymptomatically in animals, members of some non-O157 serogroups may cause enteric disease in young animals. In rabbits, EHEC O153 has been linked to a disease that resembles HUS.
Escherichia coli is a Gram negative rod (bacillus) in the family Enterobacteriaceae. Most E. coli are normal commensals found in the intestinal tract. Pathogenic strains of this organism are distinguished from normal flora by their possession of virulence factors such as exotoxins. The specific virulence factors can be used, together with the type of disease, to separate these organisms into pathotypes. Verocytotoxigenic (or verotoxigenic) E. coli (VTEC) produce a toxin that is lethal to cultured African green monkey kidney cells (Vero cells) but not to some other cultured cell types. There are two major families of verocytotoxins, Vt1 and Vt2. A VTEC isolate may produce one or both toxins. Because verocytotoxin is homologous to the shiga toxins of Shigella dysenteriae, VTEC are also called shiga toxin-producing E. coli (STEC). Enterohemorrhagic E. coli are VTEC that possess additional virulence factors, giving them the ability to cause hemorrhagic colitis and hemolytic uremic syndrome in humans. One key characteristic found in EHEC, but not exclusive to these organisms, is the ability to cause attaching and effacing (A/E) lesions on human intestinal epithelium. A/E lesions are characterized by close bacterial attachment to the epithelial cell membrane and the destruction of microvilli at the site of adherence. Some of the genes that are involved in producing A/E lesions can be used, together with the presence of the verocytotoxin, to help identify EHEC.
E. coli serotype O157:H7 is a Gram-negative, rod-shaped bacterium. The "O" in the name refers to the cell wall (somatic) antigen number, whereas the "H" refers to the flagella antigen. Other serotypes may also cause illness, though usually less severe. Other bacteria may be classified by "K" or capsular antigens. (The "O" stands for ohne Hauch [Ger. "without huff" or "without film"]; "H" for Hauch; and "K" for Kapsel.)
This is one of hundreds of serotypes of the bacterium Escherichia coli. While most strains are harmless and normally found in the intestines of mammals, this strain may produce shiga-like toxins and cause severe illness, and is a member of a class of pathogenic E. coli known as enterohemorrhagic Escherichia coli or EHEC. Often they are referred to by their toxin producing capabilities, verocytotoxin producing E. coli (VTEC) or Shiga-like toxin producing E. coli (STEC).
E. coli O157:H7 was first recognized as a pathogen as a result of an outbreak of unusual gastrointestinal illness in 1982. The outbreak was traced to contaminated hamburgers, and the illness was similar to other incidents in the United States and Japan. The etiologic agent of the illness was identified as a rare O157:H7 serotype of E. coli in 1983. This serotype had only been isolated once before, from a sick patient in 1975.
E. coli O157:H7 is markedly different from other pathogenic E. coli, as well. In particular, the O157:H7 serotype is negative for invasiveness (Sereny test), adheres through the E. coli common pilus (ECP), and does not produce heat stable or heat labile toxins. In addition, E. coli O157:H7 is usually sorbitol negative, whereas 93% of all E. coli with human origin ferment sorbitol. E. coli O157:H7 also lacks the ability to hydrolyze 4-methylumbelliferyl-β-D-glucuronide (MUG) and does not grow at 45 °C in the presence of 0.15% bile salts. Because of the latter characteristic, this serotype cannot be isolated by using standard fecal coliform methods that include incubation at 45 °C.
E. coli O157:H7 serotypes are closely related, descended from a common ancestor, divergent in plasmid content more than chromosomal content, and are no more related to other shiga toxin producing strains than any other randomly chosen E. coli serotype. E. coli O55:H7 and E. coli O157:H7 are most closely related and diverged from a common pathogenic ancestor that possessed the ability to form attaching and effacing lesions. E. coli O157:H7 serotypes apparently arose as a result of horizontal gene transfer of virulence factors.
Among these virulence factors are a periplasmic catalase and shiga-like toxins. Shiga-like toxins are iron-regulated toxins that catalytically inactivate 60S ribosomal subunits of eukaryotic cells, blocking mRNA translation and causing cell death. Shiga-like toxins are functionally identical to toxins produced by virulent Shigella species.
Strains of E. coli that express shiga-like toxins gained this ability due to infection with a prophage containing the structural coding for the toxin, and nonproducing strains may become infected and produce shiga-like toxins after incubation with shiga toxin positive strains. The prophage responsible seems to have infected the strain's ancestors fairly recently, as viral particles have been observed to replicate in the host if it is stressed in some way (e.g. antibiotics). The periplasmic catalase is encoded on the pO157 plasmid, and is believed to be involved in virulence by providing additional oxidative protection when infecting the host. Serotypes involved E. coli are serotyped based on the O (somatic lipopolysaccharide), H (flagellar) and K (capsular) antigens. Serotypes known to contain EHEC include E. coli O157:H7, the non-motile organism E. coli O157:H-, and members of other serogroups, particularly O26, O103, O111 and O145 but also O91, O104, O113, O117, O118, O121, O128 and others. E. coli O157:H- is closely related to E. coli O157:H7, but it not simply a nonmotile version of this organism; it also has a distinctive combination of phenotypic and virulence features. Serotyping alone is not enough to identify an organism as an EHEC; virulence factors characteristic of these organisms must also be present. E. coli O157:H7 strains are relatively homogeneous, and nearly all of these organisms carry virulence factors associated with hemorrhagic colitis and HUS. Members of other serotypes can be Enterohemorrhagic Escherichia coli Infections Last Updated: May 2009 © 2009 page 2 of 10 more heterogeneous. For example, E. coli in the serogroup O26 may have one, both or neither verocytotoxin genes, and only half of all E. coli O26 isolates in one study possessed ehx, a gene found on a plasmid associated with EHEC. Different organisms may carry distinct groups of virulence factors. For example, the virulence gene profiles of EHEC in serogroups O26 and O145 differ from each other, as well as from EHEC O157:H7. Because many virulence factors (including the verocytotoxin) are carried on plasmids or in bacteriophages, new E. coli strains that have novel disease patterns and/or are difficult to classify by the current systems can emerge. Geographic Distribution EHEC 0157:H7 infections occur worldwide; infections have been reported on every continent except Antarctica. Other EHEC are probably also widely distributed. The importance of some serotypes may vary with the geographic area.
While relatively uncommon, E. coli O157:H7 can naturally be found in the intestinal contents of some cattle. Cattle lack the shiga toxin receptor, Globotriaosylceramide, and therefore can be asymptomatic carriers of the bacterium. The prevalence of E. coli O157:H7 in North American feedlot cattle herds ranges from 0 to 60%.
EHEC are transmitted by the fecal–oral route. They can be spread between animals by direct contact or via water troughs, shared feed, contaminated pastures or other environmental sources. Birds and flies are potential vectors. In one experiment, EHEC O157:H7 was transmitted in aerosols when the distance between pigs was at least 10 feet. The organism was thought to have become aerosolized during high pressure washing of pens, but normal feeding and rooting behavior may have also contributed. The reservoir hosts and epidemiology may vary with the organism. Ruminants, particularly cattle and sheep, are the most important reservoir hosts for EHEC O157:H7. A small proportion of the cattle in a herd can be responsible for shedding more than 95% of the organisms. These animals, which are called super-shedders, are colonized at the terminal rectum, and can remain infected much longer than other cattle. Super-shedders might also occur among sheep. Animals that are not normal reservoir hosts for EHEC O157:H7 may serve as secondary reservoirs after contact with ruminants. EHEC O157:H7 is mainly transmitted to humans by the consumption of contaminated food and water, or by contact with animals, feces and contaminated soil. Person-to-person transmission can contribute to disease spread during outbreaks; however, humans do not appear to be a maintenance host for this organism. Most human cases have been linked to direct or indirect contact with cattle, but some have been associated with other species including sheep, goats (unpasteurized goat milk), pigs (dry fermented pork salami), deer (venison), horses, rabbits and birds. The infectious dose for humans is estimated to be under 100 organisms, and might be as few as 10. Foodborne outbreaks with EHEC O157:H7 are often caused by eating undercooked or unpasteurized animal products, particularly ground beef but also other meats and sausages, and unpasteurized milk and cheese. Other outbreaks have been linked to alfalfa or radish sprouts, lettuce, spinach and other contaminated vegetables, as well as unpasteurized cider. Irrigation water contaminated with feces is an important source of EHEC O157:H7 on vegetables. This organism can attach to plants, and survives well on the surface of a variety of fruits, vegetables and fresh culinary herbs. Depending on the environmental conditions, small numbers of bacteria left on washed vegetables may multiply significantly over several days. EHEC O157:H7 can be internalized in the tissues of some plants including lettuce, where it may not be susceptible to washing. Fruit flies can transmit this organism to apples, where it can multiply in wounded tissues. EHEC O157:H7 can remain viable for long periods in many food products. It can survive for at least nine months in ground beef stored at -20°C (-4°F). It is tolerant of acidity, and remains infectious for weeks to months in acidic foods such as mayonnaise, sausage, apple cider and cheddar at refrigeration temperatures. It also resists drying. Some human cases are caused by exposure to contaminated soil or water. EHEC are usually eliminated by municipal water treatment, but these organisms may occur in private water supplies such as wells. Swimming in contaminated water, especially lakes and streams, has been associated with some infections. Soil contamination has caused outbreaks at campgrounds and other sites, often when the site had been grazed earlier by livestock. The reported survival time for EHEC O157:H7 in contaminated soil varies from a month to more than 7 months. This organism can also survive for 2 months or longer in some freshwater sources, especially at cold temperatures, and it may remain viable for two weeks in marine water. One study indicated that EHEC O157:H7 is inactivated in slurry within two weeks; another suggested that it can survive up to three months. The epidemiology of other serotypes of EHEC is poorly understood. The reservoirs for EHEC O26 may be animals. Members of this E. coli serogroup have been found in various species including cattle, pigs, sheep, goats, rabbits and chickens. They are common in healthy animals as well as animals with diarrhea. Although the source of the organism is not known in many human cases, some EHEC O26 outbreaks have been foodborne (beef products and unpasteurized milk), associated with animal contact, or linked to water contaminated with feces. Possible person-to-person transmission has also been reported. VTEC O103 has been found in cattle, sheep and goats, as well as healthy and sick humans. In contrast, EHEC O157:H- has rarely been isolated from cattle and horses, and it was absent in more than 1800 fecal samples from cattle, sheep, goats and deer in Germany and the Czech Republic. However, one outbreak was foodborne (sausages), and contact with an infected cow and horse were the probable sources of infection in another outbreak. It is possible that humans are a reservoir host for this organism.Infection with E. coli O157:H7 follows ingestion of contaminated food or water, or oral contact with contaminated surfaces. It is highly virulent, with a low infectious dose: an inoculation of fewer than 10 to 100 CFU of E. coli O157:H7 is sufficient to cause infection, compared to over one-million CFU for other pathogenic E. coli strains.
A main source of infection is undercooked ground beef; other sources include consumption of unpasteurized milk and juice, raw produce and salami, and contact with infected live animals. Waterborne transmission occurs through swimming in contaminated lakes, pools, or drinking inadequately treated water. The organism is easily transmitted from person to person and has been difficult to control in child day-care centers.
E. coli O157:H7 is found on cattle farms and can live in the intestines of healthy cattle. The toxin requires highly specific receptors on the cells' surface in order to attach and enter the cell; species such as cattle, swine, and deer which do not carry these receptors may harbor toxigenic bacteria without any ill effect, shedding them in their feces, from which they may be spread to humans. Some cattle may also be so-called 'super-shedders' of the bacterium. Super-shedders may be defined as cattle exhibiting rectoanal junction colonization and excreting >103 to 4 CFU g−1 feces. Super-shedders have been found to constitute a small proportion of the cattle in a feedlot (<10%) but they may account for >90% of all E. coli O157:H7 excreted.
Carcasses and hides can become contaminated during slaughter and butchering, and organisms can be thoroughly mixed into beef when it is ground into hamburger. Bacteria present on the cow's udders or on equipment may get into raw milk. Contaminated foods look, smell, and taste the same as their normal counterparts.
United States food advocates have unsuccessfully attempted to control the spread of this illness by promoting the so-called "Kevin's Law". This law would give the United States Department of Agriculture power to shut down food processing plants that fail multiple inspections. The food processing industry vigorously opposes this proposal. Disinfection E. coli can be killed by numerous disinfectants including 1% sodium hypochlorite, 70% ethanol, phenolic or iodine–based disinfectants, glutaraldehyde and formaldehyde. This organism can also be inactivated by moist heat (121°C [250°F] for at least 15 min) or dry heat (160–170°C [320-338°F] for at least 1 hour). Foods can be made safe by cooking them to a minimum temperature of 160°F/ 71°C. Ionizing radiation or chemical treatment with a sodium hypochlorite solution may reduce or eliminate bacteria on produce. Infections in Humans Incubation Period The incubation period for disease caused by EHEC O157:H7 ranges from one to 16 days. Most infections become apparent after 3–4 days; however, the median incubation period was 8 days in one outbreak at an institution. Clinical Signs Humans can be infected asymptomatically or they may develop watery diarrhea, hemorrhagic colitis and/ or hemolytic uremic syndrome. Most symptomatic cases begin with diarrhea. Some cases resolve without treatment in approximately a week; others progress to hemorrhagic colitis within a few days. Hemorrhagic colitis is characterized by diarrhea with profuse, visible blood, accompanied by abdominal tenderness, and in many cases, by severe abdominal cramps. Some patients have a low–grade fever; in others, fever is absent. Nausea and vomiting may be seen, and dehydration is possible. Many cases of hemorrhagic colitis are self–limiting and resolve in approximately a week. Severe colitis may result in intestinal necrosis, perforation or the development of colonic strictures. Hemolytic uremic syndrome occurs in up to 16% of patients with hemorrhagic colitis. This syndrome is most common in children, the elderly and those who are immunocompromised. It usually develops a week after the diarrhea begins, when the patient is improving. Occasionally, children develop HUS without prodromal diarrhea. HUS is characterized by kidney failure, hemolytic anemia and thrombocytopenia. The relative importance of these signs varies. Some patients with HUS have hemolytic anemia and/or thrombocytopenia with little or no renal disease, while others have significant kidney disease but no thrombocytopenia and/or minimal hemolysis. Extrarenal signs including CNS involvement with lethargy, irritability and seizures are common. In more severe cases, there may be paresis, stroke, cerebral edema or coma. Respiratory complications can include pleural effusion, fluid overload and adult respiratory distress syndrome. Elevation of pancreatic enzymes or pancreatitis may also be seen. Rhabdomyolysis and myocardial involvement are rare. The form of HUS usually seen in adults, particularly the elderly, is sometimes called thrombotic thrombocytopenic purpura (TTP). In TTP, there is typically less kidney damage than in children, but neurologic signs including stroke, seizures and CNS deterioration are more common. Death occurs most often in cases with serious extrarenal disease such as severe CNS signs. Approximately 65–85% of children recover from HUS without permanent damage; however, long-term renal complications including hypertension, renal insufficiency and end-stage renal failure also occur. Residual extrarenal problems such as transient or permanent insulin-dependent diabetes mellitus, pancreatic insufficiency, gastrointestinal complications or neurological defects such as poor fine-motor coordination are possible. Communicability Person-to-person transmission occurs by the fecal-oral route. Most people shed EHEC O157:H7 for approximately 7 to 9 days; a minority can excrete this organism for 3 weeks or longer after the onset of symptoms. In a few cases, shedding may continue for several months. Young children tend to shed the organism longer than adults. Transmission is particularly common among children still in diapers.
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.
In some people, particularly children under five years of age and the elderly, the infection can cause hemolytic uremic syndrome (HUS), in which the red blood cells are destroyed and the kidneys fail. About 2–7% of infections lead to this complication. In the United States, HUS is the principal cause of acute kidney failure in children, and most cases of HUS are caused by E. coli O157:H7.Diagnostic Tests Because humans do not normally carry EHEC, clinical cases can be diagnosed by finding these organisms in fecal samples. Food and environmental samples may also be tested to determine the source of the infection. EHEC are sometimes difficult to identify. They are a minor population in the fecal flora or food. They also closely resemble commensal E. coli except in verocytotoxin production. However, the verocytotoxin alone does not necessarily identify an organism as EHEC; additional virulence factors must also be present.. Many diagnostic laboratories can detect verocytotoxin-producing E. coli (VTEC) and identify EHEC O157:H7; non-O157 EHEC strains must often be sent to a reference laboratory for identification. There is no single technique that can be used to isolate all EHEC serotypes. Selective and differential media have been developed for EHEC O157:H7, based on its lack of β-glucuronidase activity and the inability of most strains to rapidly ferment sorbitol. MacConkey agar containing 1% sorbitol (SMAC), often with cefixime and either rhamnose or potassium tellurite, is frequently used. Hemorrhagic colitis agar can be used to isolate EHEC O157:H7 from foods. Other media, including commercial chromogenic agars (e.g., rainbow agar), are also available. Because other strains of E. coli, as well as other bacteria, can grow on these media, prior enrichment for E. coli O157 aids detection, particularly in samples from food and the environment. For enrichment, samples may be cultured in liquid enrichment medium, or immunomagnetic separation (IMS) can be used to concentrate the members of serogroup O157 before plating. In IMS, magnetic beads coated with an antibody to the O157 antigen are used to bind these organisms. Colonies suspected to be EHEC O157:H7 are confirmed to be E. coli with biochemical tests, and shown to have the O157 somatic antigen and H7 flagellar antigen with immunoassays. A variety of tests including enzyme-linked immunosorbent assays (ELISAs), agglutination, PCR, immunoblotting or Vero cell assay can be used to detect the verocytotoxin or its genes. Phage typing and pulsed field gel electrophoresis can subtype EHEC O157:H7 for epidemiology; these tests are generally done by reference laboratories. Subtyping is important in finding the source of an outbreak and tracing transmission. The techniques used to identify EHEC O157:H7 can miss atypical strains of this organism, including rare sorbitol-fermenting isolates. They are also ineffective for detecting EHEC O157:H–, which ferments sorbitol and is beta-glucuronidase positive. Identification of EHEC O157:H- is laborious, but it can be done by IMS followed by plating samples onto SMAC and testing individual sorbitol-fermenting colonies to detect the O157 antigen, verocytotoxins or their genes, and/or other virulence factors. Selective media and isolation techniques have been developed for few non-O157 EHEC. IMS beads are commercially available for concentrating some common EHEC serogroups including O26, O103, O111 and O145. A selective rhamnose MacConkey medium containing cefixime and tellurite (CT-RMAC) is used to isolate and identify EHEC O26. Isolation of most non-O157 EHEC relies on screening colonies for verocytotoxin, the genes that produce this toxin and/or other virulence genes associated with EHEC. MacConkey agar or other media normally used to culture E. coli can be used to grow these organisms. Some prescreening techniques target specific serogroups or serotypes known to be associated with human EHEC disease. Techniques to identify most non-O157 EHEC are very labor-intensive, and these tests are not available at most laboratories. Immunological and nucleic acid-based tests that detect O and H antigens, verocytotoxin or various genes associated with EHEC can be used for presumptive diagnosis. These rapid tests can determine whether potential pathogens are present in samples before isolation. They include dipstick and membrane technologies, agglutination tests, microplate assays, colony immunoblotting, PCR, immunofluorescence and ELISAs. Although verocytotoxin production can aid identification, VTEC are not necessarily EHEC and additional virulence factors must usually be identified. Verocytotoxin-negative derivatives of the EHEC may occasionally be found by the time HUS develops. The results from rapid tests are confirmed by isolating the organism. In humans, EHEC may not be found in feces after one week. Serology is also valuable in humans, particularly later in the course of the disease when EHEC are difficult to find. Indirect ELISAs can detect antibodies to EHEC O157:H7 for months after infection. Cross-reactions with other bacteria can be seen.
A stool culture can detect the bacterium, although it is not a routine test and so must be specifically requested. The sample is cultured on sorbitol-MacConkey (SMAC) agar, or the variant cefixime potassium tellurite sorbitol-MacConkey agar (CT-SMAC). On SMAC agar O157 colonies appear clear due to their inability to ferment sorbitol, while the colonies of the usual sorbitol-fermenting serotypes of E. coli appear red. Sorbitol nonfermenting colonies are tested for the somatic O157 antigen before being confirmed as E. coli O157. Like all cultures, diagnosis is time-consuming with this method; swifter diagnosis is possible using PCR techniques. Newer technologies using fluorescent and antibody detection are also under development.
E. coli O157:H7 infection is nationally reportable in the USA and Great Britain, and is reportable in most US states. It is also reportable in most states of Australia including Queensland.
While fluid replacement and blood pressure support may be necessary to prevent death from dehydration, most victims recover without treatment in five to 10 days. There is no evidence that antibiotics improve the course of disease, and treatment with antibiotics may precipitate hemolytic uremic syndrome. Antidiarrheal agents, such as loperamide (imodium), should also be avoided as they may prolong the duration of the infection.
Hemolytic-uremic syndrome is a life-threatening condition usually treated in an intensive care unit. Blood transfusions and kidney dialysis are often required. With intensive care, the death rate for hemolytic uremic syndrome is 3–5%.
Certain novel treatment strategies, such as the use of anti-induction strategies to prevent toxin production and the use of anti-Shiga toxin antibodies, have also been proposed. Treatment Treatment of hemorrhagic colitis is supportive, and may include fluids and a bland diet. Antibiotics are controversial and are usually avoided: they do not seem to reduce symptoms, prevent complications or decrease shedding, and they may increase the risk of HUS. The use of antimotility (antidiarrheal) agents in hemorrhagic colitis also seems to increase the risk for developing HUS. Patients with complications may require intensive care including dialysis, transfusion and/or platelet infusion. Patients who develop irreversible kidney failure may need a kidney transplant.
The pathogen results in an estimated 2,100 hospitalizations annually in the United States. The illness is often misdiagnosed; therefore, expensive and invasive diagnostic procedures may be performed. Patients who develop HUS often require prolonged hospitalization, dialysis, and long-term followup.
Frequent hand washing, especially before eating or preparing food, and good hygiene are important in preventing transmission from animals and their environment. Hand washing facilities should be available in petting zoos and other areas where the public may contact livestock, and eating and drinking should be discouraged at these sites. To protect children and other household members, people who work with animals should keep their work clothing, including shoes, away from the main living areas and launder these items separately. Two children apparently became infected with EHEC O157:H7 after contact with bird (rook) feces, possibly via their father’s soiled work shoes or contaminated overalls. After a number of outbreaks associated with camping in the U.K., the Scottish E. coli O157 Task Force has recommended that ruminants not be grazed on land for at least three weeks before camping begins. Techniques to reduce microbial contamination during slaughter and meat processing can reduce the risk of EHEC from this source. Screening and control programs have been established for EHEC O157:H7 in meat. To prevent cross-contamination during food preparation, consumers should wash their hands, counters, cutting boards, and utensils thoroughly after they have been in contact with raw meat. Meat should be cooked thoroughly to kill E. coli. Unpasteurized milk or other dairy products and unpasteurized juices should be avoided. Water that may be contaminated should not be used to irrigate vegetable crops, and untreated manure/ effluents should not be used on fruits or vegetables that will be eaten raw. Post-harvest measures include thorough washing of vegetables under running water to reduce bacterial numbers. Vegetables can also be disinfected with a dilute chlorine solution. It is safest to wash vegetables immediately before use; under some environmental conditions, populations of bacteria can build up again after Enterohemorrhagic Escherichia coli Infections Last Updated: May 2009 © 2009 page 5 of 10 a few days. EHEC carried internally in plant tissues are difficult to destroy except by irradiation or cooking. Contamination of public water supplies is prevented by standard water treatment procedures. Livestock-should be kept away from private water supplies. Microbiological testing can also be considered. To the extent possible, people should avoid swallowing water when swimming or playing in lakes, ponds and streams. Good hygiene, careful hand-washing and proper disposal of infectious feces can reduce person-to-person transmission. Thorough hand washing is especially important after changing diapers, after using the toilet, and before eating or preparing food. Bed linens, towels and soiled clothing from patients with hemorrhagic colitis should be washed separately, and toilet seats and flush handles should be cleaned appropriately. In some areas, regulations may prohibit infected children from attending daycare or school until they are no longer shedding organisms. Some authors suggest that isolating infected children from their young siblings or other young household members can significantly decrease the risk of secondary spread.
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