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Epidemiologic Notes and Reports Isolation of E. coli O157:H7 from Sporadic Cases of Hemorrhagic Colitis -- United States

As part of its commemoration of CDC's 50th anniversary, MMWR is reprinting selected MMWR articles of historical importance to public health, accompanied by current editorial notes. Reprinted below is a report published November 5, 1982, which was the first in MMWR to describe diarrheal illness attributable to Escherichia coli serotype O157:H7 infections.

Since the beginning of August 1982, stool isolates of Escherichia coli serotype O157:H7 have been identified at CDC from specimens obtained from four patients in two states. Three of four patients had an unusual bloody diarrheal illness; each illness began suddenly with severe crampy abdominal pain followed within 24 hours by watery diarrhea, which subsequently became markedly bloody. One patient underwent a laparotomy to rule out appendicitis. All patients recovered within 7 days without complications or specific therapy. In one instance, E. coli O157:H7 was isolated from the stool of a patient's spouse. This fourth patient had abdominal cramps and non-bloody diarrhea. Since early August, 25 additional sporadic cases of this unusual illness have been reported to CDC, but appropriately collected stool specimens were available in only two of these. E. coli O157:H7 was not isolated from either specimen. The four patients with sporadic cases in which E. coli was isolated from stools and 24 of the remaining 25 patients with sporadic cases had eaten hamburgers from a variety of sources (including homes and/or local or national-chain restaurants) within the week before they became ill.

Examination of stool samples from sporadic cases of this recently recognized diarrheal illness, currently designated "hemorrhagic colitis," began at CDC after E. coli O157:H7 was isolated from patients in two separate outbreaks of this illness earlier this year in Oregon and Michigan. Illness was associated with eating hamburgers at restaurants of one national chain.

Hemorrhagic colitis appears to be a distinct clinical entity, characterized by severe crampy abdominal pain, grossly bloody diarrhea, little or no fever, a characteristic barium-enema finding of marked edema involving the cecum, ascending and/or transverse colon, and the absence of usual pathogens in stool.

Reported by: RR Uyeyama, MD, Good Samaritan Hospital, San Jose, SB Werner, MD, S Chin, MD, State Epidemiologist, California Dept of Health Svcs; SF Pearce, MD, CL Kollip, MD, Portland Adventist Medical Center, Portland, LP Williams, DVM, JA Googins, MD, State Epidemiologist, Oregon State Health Div; Enteric Diseases Br, Div of Bacterial Diseases, Center for Infectious Diseases, CDC.

editorial note: The diagnoses of hemorrhagic colitis are based on the typical clinical presentation and isolation of E. coli O157:H7 from the stool specimens. Early stool collection (within 4 days after onset of illness and before any antibiotic exposure) is crucial for detecting the E. coli, so physicians encountering typical cases need to ensure that stool samples are obtained and a portion held frozen (preferably at -70 C {-94 F} or on dry ice) while their laboratories perform routine examinations for Salmonella, Shigella, Campylobacter, Yersinia, and parasites. If these test results are negative, arrangements can be made through the state epidemiologist and state laboratory director to look for E. coli O157:H7 in the frozen specimen. Those state laboratories that do not have the antisera to identify E. coli O157:H7 may wish to send either the whole frozen stool or 10 picks (if possible) of E. coli colonies to CDC. This strain of E. coli O157:H7 does not ferment sorbitol, and this biochemical property may facilitate screening for this serotype. Further studies are under way at CDC to better characterize the epidemiology of hemorrhagic colitis, the reservoir of E. coli O157:H7, and serologic methods to confirm infection.

Epidemiologic investigation of the outbreaks showed that one source of E. coli O157:H7 is hamburger. Other enteric diseases, such as salmonellosis, have been reported following consumption of hamburger (1). Careful handling and adequate cooking of raw meat products should minimize or eliminate the risk of contracting infectious diseases from this source. reference

  1. Fontaine RE, Arnon S, Martin WT, et al. Raw hamburger: an interstate common source of human salmonellosis. Am J Epidemiol 1978;107:36-45.

    Editorial Note

Editorial Note 1997: A journey of a thousand miles must begin with a single step.

  • Lao-Tzu, Chinese philosopher

This description of four persons with diarrheal illness attributable to E. coli O157:H7 was among the earliest published references to this pathogen and the first report of this problem to be published in MMWR. From this modest beginning, E. coli O157:H7, the most commonly identified member of a group of organisms that is now referred to as the Shiga toxin-producing E. coli (STEC), has become one of the best-known emerging pathogens and one that is considered prototypic for the current paradigm of foodborne diseases in the United States (1). Over its 15-year history, E. coli O157:H7 has evolved as a major problem for primary-care practitioners, pediatric nephrologists, infectious-disease physicians, public health authorities, and those in the child-care setting and the food industry. In the process, the public health imperative to address this problem has influenced the careers of many of CDC's Epidemic Intelligence Service officers. For example, during a 2-year training assignment to the Washington State Department of Health, this author devoted a substantial amount of time investigating outbreaks attributed to this organism and systematically interviewing the hundreds of persons in that state with sporadic cases of E. coli O157:H7 infection (2).

As all successful public health practitioners and clinicians quickly learn, there is no better way to develop a feel for a disease and its risk factors than by talking to patients with the illness. In reading the MMWR article of 1982, it is striking to discover how many of the now classic features of E. coli O157:H7 infection could be identified in those four initial patients -- these features are typical of hemorrhagic colitis, including abdominal cramping and nonbloody diarrhea rapidly progressing to bloody diarrhea in the absence of prominent fever. In addition, the report notes the occurrence of nonbloody, culture-confirmed disease; the suggestion of person-to-person transmission (which was subsequently confirmed); the great potential for misdiagnosis and inappropriate clinical procedures (in this case laparotomy); and spontaneous recovery without specific therapy, obviating the need for antimicrobial agents (3). The report also highlights another critical issue -- the failure to collect appropriate specimens to diagnose this and other enteric pathogens. Even today, with the increasingly high profile of this disease, clinicians often fail to consider the diagnosis of E. coli O157:H7 or to collect appropriate specimens, and laboratories often fail to use necessary screening techniques for its identification.

However, one element of this disease was not mentioned in the 1982 report. None of the four patients developed hemolytic uremic syndrome (HUS) nor was it mentioned as a potential complicating factor. HUS is now recognized to occur in 5%-10% of reported cases of E. coli O157:H7; it occurs most commonly in patients with this disease who are aged less than 5 years (3). Remarkably, the outbreaks in Oregon and Michigan early in 1982, which led to the initial identification of E. coli O157:H7, are among the only ones recognized in which none of the case-patients developed HUS, probably because few of the illnesses occurred in children (4). It was not until the following year that the association between E. coli O157:H7 and HUS was first reported (5,6). However, two outbreaks of HUS had occurred earlier in North America before this association was recognized, including one in 1980 outside of Toronto in association with apple juice (7) and one in 1982 in Sacramento (8). The history of this problem highlights the need for rapid reporting and thorough evaluation of clusters of unknown etiology. These two outbreaks probably were due to infections with E. coli O157:H7, because in North America, most cases of HUS -- the most common cause of acute renal failure of childhood -- are associated with this infection (9). The combination of the severity of the clinical syndrome, the frequency of severe complications, and the lack of specific therapeutic interventions account for the perception of E. coli O157:H7 as one of the most feared emerging pathogens.

The initial outbreaks of E. coli O157:H7 were associated with two outlets of the same fast-food chain, and illness was linked to undercooked hamburgers. The MMWR report mentioned that most of the persons with sporadic hemorrhagic colitis had eaten hamburgers from a variety of sources. Since this report, many other E. coli O157:H7 outbreaks, including a large outbreak in 1993 in the Pacific Northwest (10), have been linked to ground beef. Although cattle are known to be a major reservoir for this pathogen, the ecology of the organism in animals is poorly understood.

However, accumulating experience has established a diversity of sources for E. coli O157:H7, including apple juice and cider, raw vegetables such as lettuce, raw milk, and processed foods such as salami (1). Some recent outbreaks have been related to low-level contamination of widely dispersed products, which are more available as a result of advances in the food production and distribution industry. In such instances, outbreaks are marked by small numbers of cases occurring over wide geographic areas. These outbreaks are difficult to detect and investigate. Expanded use of subtyping methods, such as pulsed-field gel electrophoresis for seemingly sporadic cases of E. coli O157:H7, will increase the likelihood of detecting diffuse outbreaks (11). Although this will expand knowledge of this pathogen, investigation of such outbreaks is likely to further strain health department resources.

Despite the substantial gains in knowledge about E. coli O157:H7 since its recognition 15 years ago, many fundamental questions and concerns remain. For example, the reasons for the original emergence of this pathogen and for its geographic spread are not known. In recent years, the organism has become a global health problem; in 1996 alone, major outbreaks were reported in Germany and Scotland, and the largest recognized outbreak, affecting approximately 5000 persons, occurred in Japan (12). How frequent is this infection? In a recent study of 10 hospitals from all U.S. regions, E. coli O157:H7 was the second or third most commonly isolated bacterial enteric pathogen in four hospitals, and its overall isolation rate was more than one third of that for Shigella sp. (13). However, despite its frequency and the availability of inexpensive commercial tests for screening and identification, by the end of 1994 only approximately 50% of U.S. clinical laboratories were screening either all stools or bloody stools for E. coli O157:H7 (14). Because misdiagnosis can lead to unnecessary therapies and procedures and because person-to-person spread is not uncommon, stool specimens from all patients with a history of acute bloody diarrhea should be cultured for this pathogen (13).

Other issues that need to be addressed include 1) determining the public health importance in North America of other STEC -- STEC have been recognized as the cause of two outbreaks in the United States and appear to be more common than E. coli O157:H7 in other parts of the world, such as Argentina and Australia; 2) deciding whether laboratory screening approaches in the United States should be changed to identify other STEC; 3) determining why some persons develop HUS after STEC infection and others do not, and whether there is any secondary prevention for this complication; 4) identifying the best primary prevention strategy; and 5) estimating the extent to which measures such as Hazard Analysis Control Critical Point work to reduce the threat of E. coli O157:H7 to the food supply, and what other measures might be necessary. Efforts to address these and other questions are included in the President's Food Safety Initiative, which was issued in May 1997 (15). Such efforts are critical to enhance understanding of E. coli O157:H7, other known foodborne pathogens, and as yet undiscovered pathogens that will constitute the foodborne challenges of the future. 1997 Editorial Note by Stephen M Ostroff, MD, Associate Director for Epidemiologic Science, National Center for Infectious Diseases, CDC.


  1. Armstrong GL, Hollingsworth J, Morris JG Jr. Emerging foodborne pathogens: Escherichia coli O157:H7 as a model of entry of a new pathogen into the food supply of the developed world. Epidemiol Rev 1996;18:29-51.

  2. Ostroff SM, Kobayashi JM, Lewis JH. Infections with Escherichia coli O157:H7 in Washington state: the first year of statewide disease surveillance. JAMA 1989;262:355-9.

  3. Griffin PM, Tauxe RV. The epidemiology of infections caused by Escherichia coli O157:H7, other enterohemorrhagic E. coli, and the associated hemolytic uremic syndrome. Epidemiol Rev 1991;13:60-98.

  4. 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.

  5. Karmali MA, Steele BT, Petric M, Lim C. Sporadic cases of haemolytic-uraemic syndrome associated with faecal cytotoxin and cytotoxin-producing Escherichia coli in stools. Lancet 1983;1:619-20.

  6. Karmali MA, Petric M, Lim C, Fleming PC, Arbus GS, Lior H. The association between idiopathic hemolytic uremic syndrome and infection by verotoxin-producing Escherichia coli. J Infect Dis 1985;151:775-82.

  7. Steele BT, Murphy N, Arbus GS, Rance CP. An outbreak of hemolytic uremic syndrome associated with ingestion of fresh apple juice. J Pediatr 1982;101:963-5.

  8. Rogers MF, Budnick LD, Kirson I, et al. Hemolytic-uremic syndrome -- an outbreak in Sacramento, California. West J Med 1986;144:169-73.

  9. Boyce TG, Swerdlow DL, Griffin PM. Escherichia coli O157:H7 and the hemolytic-uremic syndrome. N Engl J Med 1995;333:364-8.

  10. Bell BP, Goldoft M, Griffin PM, et al. A multistate outbreak of Escherichia coli O157:H7-associated bloody diarrhea and hemolytic uremic syndrome from hamburgers: the Washington experience. JAMA 1994;272:1349-53.

  11. Stephenson J. New approaches for detecting and curtailing foodborne microbial infections. JAMA 1997;277:1337,1339-40.

  12. Izumiya H, Terajima J, Wada A, et al. Molecular typing of enterohemorrhagic Escherichia coli O157:H7 isolates in Japan by using pulsed-field gel electrophoresis. J Clin Microbiol 1997;35:1675-80.

  13. Slutsker L, Ries AA, Greene KD, Wells JG, Hutwagner L, Griffin PM. Escherichia coli O157:H7 diarrhea in the United States: clinical and epidemiologic features. Ann Intern Med 1997;126:505-13.

  14. Boyce TG, Pemberton AG, Wells JG, Griffin PM. Screening for Escherichia coli O157:H7 -- a nationwide survey of clinical laboratories. J Clin Microbiol 1995;33:3275-7.

  15. US Environmental Protection Agency/US Department of Health and Human Services/US Department of Agriculture. Food safety from farm to table: a national food-safety initiative. Washington, DC: US Environmental Protection Agency/US Department of Health and Human Services/US Department of Agriculture, 1997.

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