- Get the Facts on Hemorrhagic Colitis Caused by E. Coli
- E. Coli Infections Can Be Mild to Life-Threatening
- How Do You Acquire E. Coli Hemorrhagic Colitis?
- Symptoms and Treatment of E. Coli Hemorrhagic Colitis
- Ways to Prevent E. Coli Hemorrhagic Colitis
- Update: Sporadic Hemorrhagic Colitis
- Chronic Diarrhea, Hemorrhagic Colitis, and Hemolytic-Uremic Syndrome Associated with HEp-2 Adherent Escherichia coli in Adults Infected with Human Immunodeficiency Virus in Bangui, Central African Republic
From 1982 to 2002, a total of 350 E. coli O157 outbreaks were reported in the United States from 49 states. Despite regulatory efforts to improve the safety of the U.S. food supply, foodborne E. coli O157 outbreaks remain common. Ground beef remains the most frequently identified vehicle, and produce-associated outbreaks are commonly reported. In addition, nonfoodborne transmission routes remain prominent. Person-to-person outbreaks occur most frequently in child daycare centers. Waterborne outbreaks caused by both drinking and recreational water continue to be reported, and outbreaks due to animal contact are increasingly reported.
In January 1993, the largest E. coli O157 outbreak from ground beef was reported in 4 western states, involving >700 ill persons, mostly children; more than one quarter were hospitalized, HUS developed in 7.5%, and 4 children died (3,10). Illness was linked to eating undercooked hamburgers at a chain fast-food restaurant, prompting a recall of >250,000 hamburgers, which likely prevented many additional illnesses and deaths.
Outbreak investigations that implicated fast-food hamburgers have led to major improvements in meat safety in the U.S fast-food industry. In 1993, the U.S. Food and Drug Administration revised the Model Food Code for restaurants, with new temperature guidelines for ground beef (11). In 1994, the National Livestock and Meat Board’s Blue Ribbon Task Force developed objective measures of meat “doneness” and encouraged use of automated cooking systems (12). No fast-food hamburger-associated outbreaks have been reported since 1995, demonstrating that changes in the fast-food industry, such as carefully regulating cooking temperature of hamburgers, are both possible and effective.
In addition, outbreak investigations coupled with traceback investigations of implicated meat have identified contaminated beef lots, leading to large recalls of potentially contaminated beef (3). These recalls of up to 25 million pounds of beef (13) likely prevented many additional infections. Despite these improvements, ground beef continues to be frequently implicated in E. coli O157 outbreaks. Raw beef, especially ground beef, can be contaminated with E. coli O157 and should be cooked thoroughly to kill pathogens and handled carefully to avoid cross-contamination of other food items. As ground beef outbreaks are commonly reported from home-prepared ground beef, educational efforts should be focused on teaching consumers safer handling and cooking practices.
Outbreaks provide information about inadequacy of processing methods. For example, in 1994, an E. coli O157 outbreak due to eating commercially distributed dry-cured salami product involved 23 persons; HUS developed in 13% (14). This outbreak prompted U. S. Department of Agriculture officials to develop regulations to ensure the safety of shelf-stable fermented sausages (15); no further E. coli O157 outbreaks due to U.S.–manufactured salami have been reported since.
E. coli O157 outbreaks due to produce have become increasingly common. While half of produce-associated outbreaks were due to kitchen-level cross-contamination, which calls for further prevention efforts targeting food preparers, the other half were due to produce already contaminated with E. coli O157 before purchase, including lettuce, sprouts, cabbage, apple cider, and apple juice (16–20). These produce items could have become contaminated in the field from manure or contaminated irrigation water; during processing due to contaminated equipment, wash water, or ice or poor handling practices; during transport; or through contaminated storage equipment. Washing produce with water or a chlorine-based solution reduces E. coli O157 counts only modestly (21,22); therefore, once consumers obtain contaminated produce intended for raw consumption, little can be done to prevent illness. Efforts by industry to decrease contamination of sprouts have had limited success (23,24). Until effective measures for preventing E. coli O157 contamination of produce items such as lettuce, cabbage, and sprouts can be implemented, consumers should be educated about potential risk of consuming these items raw. Further regulatory and educational efforts are needed to improve the safety of produce items.
In 1996, a large E. coli O157 outbreak occurred in 3 western states and British Columbia, involving 70 illnesses, mostly children; more than one third of patients were hospitalized, HUS developed in 20%, and 1 child died (20). Illness was attributable to drinking commercial unpasteurized apple juice. However, as a result of this outbreak investigation, apple cider and apple juice that are shipped interstate in the United States since 1998 are either pasteurized or, if sold raw, carry a warning label advising consumers of potential harmful bacteria in the product (25). Since 1998, only 2 outbreaks due to unpasteurized apple cider have been reported, 1 at a local fair and 1 from locally produced cider that carried a warning label.
Prevention efforts focused on hygiene are needed to reduce transmission in daycare settings. In outbreaks of other primary transmission routes, secondary cases occur, which emphasizes the importance of educating caretakers to avoid direct contact with fecal matter and to apply stringent handwashing rules.
Drinking and recreational water have the potential to infect many persons. The largest U.S. E. coli O157 outbreak occurred in 1999 at a county fair due to contaminated drinking water and involved 781 ill persons; 9% were hospitalized, HUS developed in 2%, and 2 died (26). The implicated water was from a temporary unregulated well at the fairground. Properly functioning water systems with adequate chlorine levels should protect against E. coli O157 contamination. Many U.S. households, however, receive municipal water that is not chlorinated. Further safeguards are therefore needed to ensure the safety of unchlorinated water systems and to ensure that chlorinated water systems are properly functioning. Educational efforts targeted at caretakers of young children should continue to help reduce contamination of recreational water areas by fecal matter (27,28).
Outbreaks associated with animal contact represent a newly recognized transmission route for E. coli O157 in the United States. Cattle hides may become contaminated from fecal matter. Persons touching cattle or surfaces in the cattle’s environment may contaminate their hands with E. coli O157. If hands are not washed thoroughly after contact with cattle or their environments, the bacteria can infect these persons through a hand-to-mouth route. Recent strategies published to help reduce transmission of enteric pathogens from farm animals to children include informing the public about risk for transmission of enteric pathogens from farm animals to humans, separating eating facilities from animal contact areas, and providing adequate handwashing facilities (29).
The overall decreased HUS and case-fatality rates in the last 2 decades likely represent increased reporting of less clinically severe outbreaks, especially after E. coli O157 became a reportable disease. The high HUS rate found in swimming-associated outbreaks may be due partly to the higher proportion of young children involved and their vulnerability to development of HUS. The reason for the higher HUS rate found among ground beef–related outbreaks is unclear and may reflect reporting bias. Outbreaks occurring in residential facilities such as nursing homes had a particularly high case-fatality rate, which emphasizes the need for prevention efforts, both educational and regulatory, to lower the incidence of E. coli O157 infections in such facilities.
Since 1992, molecular subtyping of E. coli O157 by pulsed-field gel electrophoresis has improved early outbreak detection. PulseNet (30), the national network for comparing molecular subtypes of common foodborne bacterial pathogens, including E. coli O157 since 1997, has greatly assisted in both identifying outbreaks and linking apparently unrelated outbreaks. Continued molecular subtyping of E. coli O157 strains from both humans and the environment will assist in detecting outbreaks and allow for identification of multistate, geographically dispersed outbreaks due to contaminated commercial products (30).
Outbreak surveillance has several limitations. E. coli O157 outbreaks captured by CDC’s surveillance system likely represent only a small proportion of outbreaks that occur. Many outbreaks go unrecognized, are classified as outbreaks of unknown etiology, and are not reported to local public health officials or CDC (31). Smaller outbreaks and outbreaks with unknown transmission routes and vehicles are less likely to be reported, and this summary likely under represents such outbreaks. Including patients with compatible clinical illness without culture confirmation is another limitation of outbreak surveillance. However, given the broad clinical spectrum of E. coli O157 infection, and the limited number of infected persons with culture-confirmed illness (5), such inclusion allows us to better assess the true public health impact of E. coli O157. In addition, outbreak reporting may not be uniform across time periods or states. Therefore, trends should be interpreted carefully, given the changing factors that may impact outbreak detection and reporting. The increased numbers of outbreaks reported since 1993 but with smaller sizes are likely due to increased awareness of disease, improved diagnostics, increased E. coli O157 testing, and improved outbreak detection through molecular subtyping.
Outbreak investigations, especially for emerging pathogens such as E. coli O157, are critical for better understanding these pathogens’ epidemiology, which affect policy and behavior changes. While a summary of outbreaks cannot draw firm conclusions on disease trends, illustration of transmission routes, food vehicles, outbreak size, and clinical outcomes over time empowers public health officials, regulatory agencies, and health educators to target appropriate interventions and reevaluate current prevention strategies.
If you are not the author of this article and you wish to reproduce material from it in a third party non-RSC publication you must formally request permission using Copyright Clearance Center. Go to our Instructions for using Copyright Clearance Center page for details.
Authors contributing to RSC publications (journal articles, books or book chapters) do not need to formally request permission to reproduce material contained in this article provided that the correct acknowledgement is given with the reproduced material.
Reproduced material should be attributed as follows:
- For reproduction of material from NJC:
Reproduced from Ref. XX with permission from the Centre National de la Recherche Scientifique (CNRS) and The Royal Society of Chemistry.
- For reproduction of material from PCCP:
Reproduced from Ref. XX with permission from the PCCP Owner Societies.
- For reproduction of material from PPS:
Reproduced from Ref. XX with permission from the European Society for Photobiology, the European Photochemistry Association, and The Royal Society of Chemistry.
- For reproduction of material from all other RSC journals and books:
Reproduced from Ref. XX with permission from The Royal Society of Chemistry.
If the material has been adapted instead of reproduced from the original RSC publication “Reproduced from” can be substituted with “Adapted from”.
In all cases the Ref. XX is the XXth reference in the list of references.
If you are the author of this article you do not need to formally request permission to reproduce figures, diagrams etc. contained in this article in third party publications or in a thesis or dissertation provided that the correct acknowledgement is given with the reproduced material.
Reproduced material should be attributed as follows:
- For reproduction of material from NJC:
– Reproduced by permission of The Royal Society of Chemistry (RSC) on behalf of the Centre National de la Recherche Scientifique (CNRS) and the RSC
- For reproduction of material from PCCP:
– Reproduced by permission of the PCCP Owner Societies
- For reproduction of material from PPS:
– Reproduced by permission of The Royal Society of Chemistry (RSC) on behalf of the European Society for Photobiology, the European Photochemistry Association, and RSC
- For reproduction of material from all other RSC journals:
– Reproduced by permission of The Royal Society of Chemistry
If you are the author of this article you still need to obtain permission to reproduce the whole article in a third party publication with the exception of reproduction of the whole article in a thesis or dissertation.
Information about reproducing material from RSC articles with different licences is available on our Permission Requests page.
Get the Facts on Hemorrhagic Colitis Caused by E. Coli
Despite humorous portrayals in popular culture, E. coli infections are no laughing matter.
Escherichia coli, or E. coli, are bacteria that normally live inside your intestines and the intestines of animals like cattle and sheep. Most E. coli are harmless, but there are strains that cause outbreaks of food poisoning called E. coli hermorrhagic colitis.
E. coli hemorrhagic colitis (bloody diarrhea), first recognized in 1982, causes gastrointestinal bleeding as a result of inflammation of the colon, the last segment of your digestive system.
Hemorrhagic colitis related to E. coli often goes undiagnosed because people with mild cases may have diarrhea at home and never see the doctor.
“In order to diagnose it, you need to order special tests to look for a specific type of E. coli that causes the infection,” says Andelka D. LoSavio, MD, a gastroenterologist with the DuPage Medical Group in Hinsdale, Illinois.
E. Coli Infections Can Be Mild to Life-Threatening
The strain of E. coli that most commonly causes hemorrhagic colitis is E. coli 0157:H7. Other strains of E. coli may also cause the infection, but they are hard to identify.
“What makes these E. coli different from harmless E. coli is that they produce a toxin that damages the lining of the colon, causing inflammation and bleeding,” says Dr. LoSavio.
Toxins are substances made by bacteria that are poisonous to humans. The toxin made by E. coli 0157:H7 is called Shiga toxin. Shiga toxin allows the bacteria to cling to cells lining the colon and cause inflammation and cell damage.
Shiga toxin can also cause red blood cells to die. The dead cells can overwhelm the kidneys and cause a dangerous complication called hemolytic-uremic syndrome (HUS). Deadly cases of E. coli colitis are usually due to HUS and are more common in children and the elderly.
It’s hard to know how common E. coli hemorrhagic colitis is because many cases never get diagnosed. The Centers for Disease Control and Prevention (CDC) estimate there are about 73,000 cases every year in the United States.
How Do You Acquire E. Coli Hemorrhagic Colitis?
Infected animals are the main source of infection. Animals shed the bacteria through their feces. Once outside the animal, the bacteria can live for several months in contaminated water or soil.
Although cattle and sheep commonly carry the infection, so can:
Touching anything that is contaminated with bacteria and then touching your mouth, eating contaminated food, or drinking contaminated water are all common ways the infection spreads. Examples of how the disease spreads from infected animals to people include:
- Eating undercooked meat
- Drinking unpasteurized milk
- Touching an infected animal
- Drinking or swimming in contaminated water
- Eating raw contaminated fruits or vegetables
If a person gets infected, he or she can also spread an E. coli infection through feces.
Symptoms and Treatment of E. Coli Hemorrhagic Colitis
“Inflammatory bowel diseases like ulcerative colitis and Crohn’s disease can also cause bloody diarrhea, but they are long-lasting diseases. E. coli colitis usually clears up on its own within about one week,” says LoSavio.
Symptoms of E. coli hemorrhagic colitis usually begin about three days after the bacteria get into your digestive system. Symptoms can range from mild diarrhea and cramping to severe diarrhea, abdominal pain, bloody stools, nausea, and vomiting.
“Severe diarrhea can lead to dehydration and weakness,” says LoSavio.
Symptoms usually last for 5 to 10 days, and most people get better by just taking it easy and drinking plenty of fluids. But serious cases do occur, and HUS is a rare but dangerous complication.
Symptoms of HUS are decreased urine output and dark-colored urine.
“Antibiotics may be used in severe cases, but there is some evidence that antibiotic treatment may increase the risk of HUS,” says LoSavio. A study published in January 2012 in the Pediatric Infectious Disease Journal found that the use of bactericidal antibiotics, such as penicillins or cephalosporins, was associated with the development of HUS.
“The best advice is to call your doctor anytime you have bloody diarrhea. Also call your doctor anytime diarrhea is making you weak and dehydrated and anytime you have diarrhea with fever.”
Ways to Prevent E. Coli Hemorrhagic Colitis
Try these strategies for preventing E. coli hemorrhagic colitis:
- Cook all your meat thoroughly until juices run clear, especially any ground beef.
- Avoid eating meat that is pink inside.
- Do not drink unpasteurized milk or apple cider.
- Do not drink untreated water.
- Do not eat cheese or other dairy products that are unpasteurized.
- Wash your hands after touching cattle, sheep, pigs, goats, rabbits, or chickens.
- Wash your hands before preparing or eating food.
Additional reporting by Christine Gordon
Update: Sporadic Hemorrhagic Colitis
Persons using assistive technology might not be able to fully access information in this file. For assistance, please send e-mail to: . Type 508 Accommodation and the title of the report in the subject line of e-mail.
In 1983, CDC reported on investigations in Michigan and Oregon of two 1982 outbreaks of a gastrointestinal illness designated hemorrhagic colitis (1). The illness was caused by a previously unrecognized pathogen, Escherichia coli O157:H7. Since August 1982, sporadic cases of this illness have been reported to CDC, and stool specimens have been examined from patients meeting the following case definition: a person with bloody diarrhea, abdominal cramps, and low-grade or no fever, whose stool culture is negative for recognized pathogens including Salmonella, Shigella, Campylobacter, and Yersinia and for ova and parasites.
During 1983, stool specimens were examined from 35 ill persons in 16 states. E. coli O157:H7 was identified in 10 specimens collected a mean of 4.7 days after onset of illness. The culture-negative specimens were collected a mean of 7.6 days after onset. Culture-positive specimens were received from Wisconsin (three), California (two), Alabama, Florida, Illinois, Massachusetts, and Minnesota (one each). Patients ranged in age from 2 to 80 years (median 15 years), and both sexes were equally affected. The average duration of illness was 10 days, and nine of the 10 patients were hospitalized. Barium enemas of two patients revealed spasm in one and “thumbprinting” in the ascending colon in the other. Sigmoidoscopy performed in two other patients revealed erythema, edema, and friable mucosa. None of the patients required transfusions, and four were treated with antibiotics. Reported by WE Birch, DVM, State Epidemiologist, Alabama Dept of Public Health, JJ Sacks, MD, Acting State Epidemiologist, Florida Dept of Health & Rehabilitative Svcs; J Chin, MD, State Epidemiologist, California State Dept of Health Svcs; BJ Francis, MD, State Epidemiologist, Illinois Dept of Public Health; NJ Fiumara, MD, State Epidemiologist, Massachusetts Dept of Public Health; AG Dean, MD, Minnesota State Dept of Health; JP Davis, MD, State Epidemiologist, Wisconsin State Dept of Health and Social Svcs; Enteric Diseases Br, Div of Bacterial Diseases, Center for Infectious Diseases, CDC.
Editorial Note: The frequency with which E. coli O157:H7 causes hemorrhagic colitis in the United States is unknown. Isolation of this pathogen from 29% of submitted specimens suggests that it is an important cause of bloody diarrhea in patients in whom no other pathogens are detected. The organism is cleared rapidly from the stool (1); since the stool specimens were collected earlier for culture-positive cases than for culture-negative cases, E. coli O157:H7 may also have been the responsible pathogen in some of the culture-negative cases.
Disease caused by E. coli O157:H7 has not been limited to the United States nor to gastrointestinal manifestations. Sporadic cases of hemorrhagic colitis were also identified in Canada during 1983 (2). Three of these patients subsequently developed hemolytic-uremic syndrome. E. coli O157:H7 was isolated from stools of two of these patients and from the stools of two ill siblings of the third patient, who had typical symptoms of hemorrhagic colitis before developing hemolytic-uremic syndrome.
Since early stool collection is important for identifying this organism, physicians encountering typical cases should obtain the specimen as quickly as possible and then hold a portion frozen while their laboratories perform examinations for other recognized pathogens. If these test results are negative, arrangements can be made through state epidemiologists and state laboratory directors to examine the frozen portion of the specimen for E. coli O157:H7.
Although the outbreak cases were caused by eating hamburger products, no common exposures have yet been identified among sporadic cases. The sources of E. coli O157:H7 for sporadic cases are currently under investigation through an ongoing case-control study.
Riley LW, Remis RS, Helgerson SD, et al. Hemorrhagic colitis associated with a rare Escherichia coli serotype. N Engl J Med 1983;308:681-5.
Sporadic cases of hemorrhagic colitis associated with Escherichia coli O157:H7–Calgary, Alberta. Canada Diseases Weekly Report 1983;9:181-4.
Disclaimer All MMWR HTML documents published before January 1993 are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.
**Questions or messages regarding errors in formatting should be addressed to [email protected]
Page converted: 08/05/98
Chronic Diarrhea, Hemorrhagic Colitis, and Hemolytic-Uremic Syndrome Associated with HEp-2 Adherent Escherichia coli in Adults Infected with Human Immunodeficiency Virus in Bangui, Central African Republic
In human immunodeficiency virus (HIV)-infected adults from the Central African Republic, the occurrence of chronic diarrhea due to HEp-2 adherent Escherichia coli (EAEC) harboring virulence markers (eaeA, BFP, EAF, astA determinant of EAST/1, positive FAS test, enteropathogenic E. coli O serogroup) was shown to be associated with AIDS. We also show that EAEC that produce verotoxin (Stx2) but do not harbor the genetic markers for classical enterohemorrhagic E. coli are involved in hemorrhagic colitis and hemolytic-uremic syndrome in patients with HIV.
The Central African Republic is strongly affected by the human immunodeficiency virus (HIV) epidemic (24). Nearly 72% of the adults hospitalized with AIDS present initially with chronic diarrhea (CD) (14). Between 1996 and 1999 we used phenotypic (14) and genotypic assays to study 88 HIV-infected adults hospitalized in Bangui and their matched controls to determine the clinical significance of diarrheagenic Escherichia coli (7, 8, 9, 10, 12, 16, 22, 25, 27, 29, 31, 32, 34, 35). The methods were as previously described (14). To be included in the study, the patients had to be HIV positive and aged 18 or over, have CD (3 or more loose watery stools per day for at least 14 days ), have E. coli in a stool sample, and give informed consent. Each patient was matched with a control recruited from among the neighbors and family members of the patient. The matching criteria dictated that the control be aged within 5 years of the patient’s age and of the same sex. The recruitment criteria for the matched controls were as follows: testing positive for HIV antibodies, having had no diarrhea on the day of recruitment or during the previous month, and having E. coli in their stools on the day of recruitment. All controls gave informed consent to participate.
HEp-2 adherent E. coli (EAEC) (5, 28) with localized adherent (LA), aggregative adherent (AA), or diffuse adherent (DA) patterns were more common in the patients (P < 10−5) than in the controls (Table 1). Some EAEC exhibited a strong LA pattern (16 patients versus no control) in which >20% of the randomly selected cells had attached bacteria (11, 19). These LA strains with a strong LA pattern were associated with CD, especially when the assays used to identify enteropathogenic E. coli (EPEC) virulence factors yielded positive results (eaeA, EPEC adherence factor plasmid, bundle-forming pili PCR, and fluorescent actin staining test) (P < 10−5), and all belonged to known EPEC O serogroups (P = 0.0001). The isolation of enteroaggregative E. coli (EAggEC) was strongly correlated with the presentation of CD (P < 10−5). The difference in the isolation rates of EAEC strains exhibiting DA between patients and controls was only significant when the presence of the astA gene encoding EAST/1 was considered (P = 0.016); astA was located on 7- to 40-kb plasmids.
Interestingly, all of the enteric bacteria isolated from 42 patients (86% of the 49 patients with severe immunodepression) harboring EAEC with virulence factors were E. coli (Table 2). In contrast, in the 39 patients who had no EAEC or harbored EAEC with no virulence factor (Table 2) and in controls (data not shown), E. coli never represented more than 50% of the isolated enteric bacteria. This strongly suggests that some EAEC strains are diarrheagenic pathogens. Thus, colony hybridization assays under high-stringency conditions were carried out retrospectively on archived filters prepared from stools streaked onto nonselective medium to determine the percentage of colonies that harbored eaeA and astA. These stool samples were taken from 24 patients (7 carrying EPEC clones identified by the presence of eaeA, 13 harboring astA-positive EAggEC, and 4 harboring astA-positive diffusely adhering E. coli ) and 12 controls. No hybridization was observed in controls. Results showed that 90 to 100% of the isolated bacteria hybridized with the eaeA probe (18) in the 7 patients carrying EPEC clones (100%) and with the astA probe (astA PCR product from EAggEC strain 17-2 ) in the 22 patients harboring astA-positive EAggEC or DAEC. Antimicrobial susceptibility tests were carried out, and accordingly, the 22 patients harboring EAEC with virulence factors (9 with LA strains, 8 with AA strains, and 5 with astA-positive DA strains) received fluoroquinolones for 14 days. Seven days after the end of treatment, EAEC negativation of cultures was associated with complete resolution of diarrhea in 17 patients (77%; 9 with LA strains, 5 with AA strains, and 5 with DA strains). This observation provides additional evidence that these EAEC were etiologic factors of CD.
During this study, the Central African Republic was afflicted with epidemics of hemorrhagic colitis (HC) and hemolytic-uremic syndrome (HUS) (13, 15). The eight patients afflicted with both HC and HUS presented pure cultures of EAEC. Non-EPEC serogrouped LA clones producing both verotoxin (20) (Stx2 alone according to PCR tests) and hemolysin were isolated from the stools of one patient. All of the isolates were negative for the enterohemorrhagic E. coli (EHEC) plasmid marker ehec-hly (33) and for the PCR detection of EHEC and EPEC virulence genes. They did not hybridize with the EHEC probe (23) or the EAF probe (26) even under low-stringency conditions and were negative in the FAS test and for invasion in the HeLa cell gentamicin protection assay (2). They all harbored two plasmids (5 and 70 kb) that did not hybridize with an stx2 probe that reacts only with total cellular DNA. These results indicated that the stx2 gene was present on the chromosome. In the seven other patients, we isolated EAEC that produced the verotoxin (Stx2 alone according to the PCR analysis). These clones showed a mixed adherence pattern, predominated by AA. In six of these patients, isolates showed AA and also typical LA, and isolates from two patients produced hemolysin and gave negative results in the PCR analyses for the EHEC plasmid marker ehec-hly (33). In the seventh patient, isolates showed a combination of AA and LA patterns and an intercalated DA pattern. All of the clones gave negative results by PCR for the detection of virulence markers associated with EHEC, EPEC, DAEC, and EAggEC. They did not hybridize with the eaeA (18) or EHEC (23) probes, even under low-stringency conditions. Southern blot analysis indicated that the stx2 gene was present on the chromosome. Plasmid profile analysis and antimicrobial susceptibility testing indicated that strains from the seven patients were epidemiologically unrelated. Taq cycle sequencing (21, 30) showed that the B-subunit gene of the toxin stx2 was 100% homologous to the stx2 B gene from the O157:H7 strain EDL933 (17) and from the O157:H7 and O157:H− strains recently isolated in the region (13, 15). Although these isolates did not contain the classical EHEC markers (such as the eaeA gene) and were negative in the FAS test, they can be classified as EHEC because they were all isolated from HC and HUS and all produced an Stx2. In immunocompetent subjects, Stx2 production alone does not confer human pathogenicity (27). The Stx2-positive EAEC described in this study are thought to colonize the intestinal mucosa as efficiently as the eaeA-positive EHEC. This may involve unknown adhesins (the HEp-2 adherence test is a useful tool in this case for identifying potential virulent strains of E. coli), or it may illustrate that Stx2-producing E. coli with reduced virulence have a greater potential for producing HC and HUS in HIV-infected persons with enteric immune defects than in healthy individuals.
View this table:
- View inline
- View popup
HEp-2 adherent E. coli strains isolated from HIV-infected adults with and without diarrheaa
View this table:
- View inline
- View popup
Semiquantitative assessment of E. coli isolated on nonselective BCP medium according to the immunosuppression and the diarrheagenic E. coli in stools
This work was partially supported by grants ANRS no. 97085 and ANRS/VIHPAL no. 1277 and by the Groupe d’Etude des Infections Diarrhéiques (Réseau International des Instituts Pasteur et Instituts Associés).
- Received 2 January 2002.
- Returned for modification 21 March 2002.
- Accepted 7 May 2002.
- American Society for Microbiology