Review and Response of Enterohaemorrhagic Escherichia coli infection
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Since May, 2011, Germany had reported a significantly increasing trend on cases of enterohaemorrhagic Escherichia coli (EHEC) infection and haemolyticuraemic syndrome (HUS). Afterward a number of European countries had reported cases linked to this outbreak, and most cases had travel history to Germany. As of June 15, Germany had reported 2,518 cases of EHEC infection (without HUS) and 786 HUS cases with 38 fatalities. Other European countries had reported a total of 69 EHEC cases and 36 HUS cases leading to one fatal [1]. Approximate 70% of cases were in females and most were in the group aged 20-49 years. The pathogen was identified as enteroaggregative verocytotoxin-producing Escherichia coli O104:H4 bacterium. According to epidemiological findings, German officials announced that the vehicle of infection was contaminated bean and seed sprouts. The current event represents the largest outbreak of EHEC infection in recent years that resulted in dozens of deaths, as well as made great economic loss due to difficulties in epidemiological investigations and fail in prompt determination of the infective source. This article will introduce the domestic and international situation in epidemiology and surveillance of enterohaemorrhagic Escherichia coli infection.Keywords:
Verocytotoxin
Escherichia coli infection
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SUMMARY Between 1 January 2009 and 31 December 2012 in England, a total of 3717 cases were reported with evidence of Shiga toxin-producing E. coli (STEC) infection, and the crude incidence of STEC infection was 1·80/100 000 person-years. Incidence was highest in children aged 1–4 years (7·63/100 000 person-years). Females had a higher incidence of STEC than males [rate ratio (RR) 1·24, P < 0·001], and white ethnic groups had a higher incidence than non-white ethnic groups (RR 1·43, P < 0·001). Progression to haemolytic uraemic syndrome (HUS) was more frequent in females and children. Non-O157 STEC strains were associated with higher hospitalization and HUS rates than O157 STEC strains. In STEC O157 cases, phage type (PT) 21/28, predominantly indigenously acquired, was also associated with more severe disease than other PTs, as were strains encoding stx2 genes. Incidence of STEC was over four times higher in people residing in rural areas than urban areas (RR 4·39, P < 0·001). Exposure to livestock and/or their faeces was reported twice as often in cases living in rural areas than urban areas ( P < 0·001). Environmental/animal contact remains an important risk factor for STEC transmission and is a significant driver in the burden of sporadic STEC infection. The most commonly detected STEC serogroup in England was O157. However, a bias in testing methods results in an unquantifiable under-ascertainment of non-O157 STEC infections. Implementation of PCR-based diagnostic methods designed to detect all STEC, to address this diagnostic deficit, is therefore important.
Clinical Microbiology
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To the Editor: During the rainy season, from April to September 2003, 463 children ≤15 years of age (median 10 months) with severe diarrhea were admitted to the Pediatric Hospital of Kalembelembe in Kinshasa, the capital of the Democratic Republic of Congo. The population of the outbreak area was approximately one million.
Several children with bloody diarrhea without fever were treated. They came from six districts of Kinshasa (Bumbu, Selembao, Makala, Kimbanseke, Masina, and Ndjili). Abdominal cramps, nausea, vomiting, and dehydration were uncommon. The duration of illness ranged from 5 days to 2 weeks. Available antiparasitic drugs, trimethoprim-sulfamethoxazole, and ampicillin showed no effect against the illness. Fifty-six infants died between June and July. Symptoms of hemolytic-uremic syndrome developed in most of them.
Stool samples from 32 patients were screened for parasites, enteropathogenic bacteria, rotavirus, and adenovirus. Three samples were positive for rotavirus. In contrast, all stool cultures were positive for Escherichia coli which always grew as pure cultures on purple bromocresol agar, a nonselective medium containing lactose. The E. coli isolates appeared sorbitol negative when tested on MacConkey sorbitol; they were agglutinated by O157 and H7 antisera (Difco Laboratories, Detroit, MI) and lacked expression of β-glucuronidase. All E. coli isolates were sent to the Pasteur Institute in Bangui, Central African Republic, for further characterization. Polymerase chain reaction allowed detection of Shiga-like toxin slt-1 and slt-2 genes (1,2) in isolates from all patients. The Vero cell assay phenotypically confirmed cytotoxicity of these isolates, with most of them being seroneutralized by rabbit antisera against Shiga toxin (3). Thus, all E. coli isolates responded to the definition of enterohemorrhagic E. coli.
Before 2003, sporadic infections or outbreaks caused by enterohemorrhagic E. coli were not reported as a cause of bloody diarrhea in the Democratic Republic of Congo. A case-control study could not be performed because of political unrest in Kinshasa. Although reported outbreaks of E. coli O157 in sub-Saharan Africa have been few to date, available information indicates that the pathogen has wide geographic distribution. E. coli O157–related diarrhea outbreaks that occurred before 2003 have been reported in South Africa, Swaziland (4), and Malawi (5) in 1992; Central African Republic (6) and Kenya (7) in 1996; Cameroon in 1998 (8); and Nigeria (9) and Ivory Coast (10) in 2000. In the Central African Republic and in Zemio, a small village located on the Democratic Republic of Congo border, outbreaks of bloody diarrhea in 1996 were attributed to E. coli O157 from molecular test results (6).
Since 2001, an increasing number of cases of acute bloody diarrhea have been reported in Kinshasa between June and August. During this 2003 outbreak, an investigation could not be conducted; possible routes of transmission would include person-to-person contact related to lack of hygiene, and contaminated food and water.
In 1996 in the Central African Republic and in 1998 in Cameroon, the major contributing factors of the E. coli O157 outbreak were consumption of smoked zebu meat and contaminated drinking water. Studies of E. coli O157 carriage rates among livestock, food, and environment in this central African area might be useful in assessing the potential for future outbreaks.
Hemolytic-uremic syndrome occurs in approximately 8% of children and an unknown proportion of adults infected with E. coli O157 and can be fatal without hemodialysis. The high death rate of infants during this outbreak was linked to the lack of treatment (mainly hemodialysis) at the beginning of the epidemic. Obviously, more work is needed to better define the incidence and epidemiology of E. coli–associated diarrhea in the Democratic Republic of Congo so that optimal recommendations for preventing and managing illness can be developed.
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Abstract In August 2018, Public Health England (PHE) was made aware of five probable cases of Shiga toxin‐producing Escherichia coli (STEC) O157:H7 among individuals reporting participation in a mud‐based obstacle race. An additional four cases, identified via routine whole‐genome sequencing, were subsequently linked to the same event. Two of the nine cases were due to secondary household transmission. Despite an agreement between the event organizers and the local authority, to ensure that all livestock were removed from the site 28 days before the event, sheep were observed grazing on some of the routes taken by the runners 2 days prior to the race taking place. A retrospective review of incidents reported to PHE between 2015 and 2018 identified 41 cases of gastroenteritis associated with muddy assault course events. Of these, 25 cases were due to infection with STEC O157:H7, of which all but one were associated with outbreaks. Due to the environment in which such events take place, it is impossible to entirely remove the risk of exposure to potentially pathogenic zoonoses. However, race organizers should ensure that livestock are removed from the course 28 days before the event. They should also ensure that participants are made aware of the risk of contracting gastrointestinal disease from the environment, and to stress the importance of hand hygiene post‐event and the risk of secondary transmission, particularly to children who are at risk of developing haemolytic uraemic syndrome.
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Shiga toxin-producing E. coli (STEC) was first recognised as a food-borne pathogen in 1982, when it was isolated during two outbreaks of haemorrhagic colitis associated with undercooked burgers in the United States. Since then, STEC has become established as an important global gastrointestinal pathogen. STEC can colonise the gastrointestinal tract of wild, farmed, and domesticated animals and be shed in their faeces. Cattle are considered the most important reservoir for STEC in humans; infection in cattle is non-pathogenic. Transmission to humans can occur as a result of direct contact with STEC-contaminated faecal material, from handling or petting animals or by exposure to faecally contaminated soil or vegetation during recreational or occupational activities. Exposure can also occur from consumption of contaminated food or water or via person to person transmission. Reports of STEC infection in Scotland increased markedly in the mid 1990's and rates remain high when compared to other UK and European countries. In 2016 the overall rate of STEC in Scotland was 4.6 per 100,000, with the highest incidence in individuals aged under 16 years. In comparison, the 2015 rate for the UK was 2.05 per 1 00 000 and for the EU was 1.27 per 1 00 000. Serotype O157 continues to be the most frequently identified serotype in Scotland accounting for 75% of culture confirmed cases in 2016. The number of non-O157 infections has increased steadily in recent years, partially explained by changes in diagnostic practices. Among the non-O157 isolates, STEC O26 was the most common accounting for 19% in 2016. Clinical presentation ranges from asymptomatic infection to mild non-bloody diarrhoea, through bloody diarrhoea and haemorrhagic colitis to haemolytic uraemic syndrome (HUS), thrombotic microangiopathy and, in a small number of cases, death. HUS develops in approximately 10%–15% of E. coli O157 cases, with the highest rates in those under 15 years or over 65 years of age, HUS mortality is reported to be between 3% and 5%. Among the 2016 STEC cases in Scotland with enhanced surveillance information, 35% required hospitalisation.
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From May through July 2011, Germany experienced a large outbreak of Shiga toxin-producing Escherichia coli (STEC) O104:H4 infection. Our objective was to identify the prevalence of STEC O104:H4 carriers in households in highly affected areas, the rate of secondary household transmissions, and the duration of long-term shedding.In a cross-sectional study, we recruited case and control households to determine STEC household prevalence. We then conducted a prospective cohort study (households with ≥ 2 members and ≥ 1 case) to determine rates of household transmission and shedding duration.For part 1, we recruited 57 case households (62 case patients and 93 household contacts) and 36 control households (89 household members). We only detected cases in previously known case households and identified 1 possible adult-to-adult household transmission. For part 2, we followed 14 households and 20 carriers. No secondary household transmission was detected in the prospective follow-up period. In 1 adult carrier, shedding lasted >7 months. However, the median estimated shedding time was 10-14 days (95% confidence interval, 0-33 days). Three carriers showed intermittent shedding.The prevalence of STEC O104:H4 carriers even in highly affected areas appears to be low. Despite prolonged shedding in some patients, secondary adult-to-adult household transmissions seem to be rare events in the postdiarrheal disease phase.
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Box 12.1 An unusual epidemic of pneumonia On the 21st of February 2003, a doctor from southern China visited Hong Kong and stayed one night in a local hotel. Unwell for several days before the trip, he became seriously ill and the next day was admitted to a hospital with severe pneumonia; he died 10 days later. Before admission he had infected numerous people who came into contact with him, including his own family (wife, daughter, sister and brother-in-law) and 16 guests or visitors to the hotel. Some of the hotel guests left Hong Kong for Singapore, Hanoi and Toronto and outbreaks in those areas rapidly followed. Within a month large outbreaks arose in several Hong Kong hospitals, affecting staff, students, patients and visitors. As family members became infected they infected others and the disease began to spread in the community. On the 12th of March 2003, the World Health Organization issued a global alert on atypical pneumonia, called severe acute respiratory syndrome (SARS). By late March a huge outbreak in a Hong Kong housing estate was traced back to a patient discharged from one of the affected hospitals. In Hong Kong there were 1,755 cases and 300 deaths (case fatality rate, CFR = 17%), including 8 fatalities among the 386 health workers affected. The high-rise housing estate had 329 cases and 42 deaths. Hong Kong health authorities quarantined 493 households with 1,262 people, traced 26,520 contacts, and screened 36.3 million travellers. Globally, public health organisations collaborated to identify the organism, devise diagnostic tests, introduce control measures and stop the epidemic by August 2003 after 8,422 cases and 916 deaths worldwide(Chan-Yeung and Yu, 2003).
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Abstract In 1992, a large outbreak of bloody diarrhea caused by Escherichia coli O157 infections occurred in southern Africa. In Swaziland, 40,912 physician visits for diarrhea in persons ages >5 years were reported during October through November 1992. This was a sevenfold increase over the same period during 1990-91. The attack rate was 42% among 778 residents we surveyed. Female gender and consuming beef and untreated water were significant risks for illness. E. coli O157:NM was recovered from seven affected foci in Swaziland and South Africa; 27 of 31 patient and environmental isolates had indistinguishable pulsed-field gel electrophoresis patterns. Compared with previous years, a fivefold increase in cattle deaths occurred in October 1992. The first heavy rains fell that same month (36 mm), following 3 months of drought. Drought, carriage of E. coli O157 by cattle, and heavy rains with contamination of surface water appear to be important factors contributing to this outbreak.
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Infections and life-threatening complications due to verotoxin-producing Escherichia coli (VTEC) have been increasingly recognized as a public health problem in recent years. Through enhanced surveillance in Alberta, Canada, and in Scotland, 1,993 cases of VTEC infection and 115 cases of hemolytic-uremic syndrome (HUS) were detected in 1987-1991 in a combined population of more than 7.5 million; there were 24 deaths. The mean annual rates of VTEC infection were 12.1/100,000 and 2.0/100,000 for Alberta and Scotland, respectively. One case of HUS occurred for every 14 (Scotland) to 19 (Alberta) cases of VTEC infection. Rates of VTEC infection were highest among children < 5 years of age, while rates of resultant hospitalization were highest among the elderly. Male-to-female ratios for patients with VTEC infection varied with the age group. The incidence of this infection was highest in the summer: 64.0%-81.7% of cases occurred between May and September. Hamburger was the most common source reported. Unexplained geographic variation in prevalence was evident in both Alberta and Scotland. Most cases were sporadic, although several community and point-source outbreaks were identified in Scotland. HUS exhibited similar epidemiological patterns. Infections with VTEC impose a substantial preventable clinical and public health burden. Routine monitoring of these infections is considered worthwhile in order to elucidate their epidemiology and modes of transmission and ultimately to control them more effectively.
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Escherichia coli O157:H7 infection became a reportable condition in Wisconsin on April 1, 2000; previously cases were voluntarily reported by physicians and laboratories. During 1992 through 1999, 1333 cases of E. coli O157:H7 infection occurred in Wisconsin residents and were reported to the Wisconsin Division of Public Health. During this interval, the highest age-specific mean annual incidence, 13.2 cases per 100,000 population, occurred in persons 3 to 5 years old. Only 28% of patients with reported cases identified bloody diarrhea among their signs and symptoms. Of reported cases, 17% (231/1333) were involved in the eight outbreaks investigated during this interval. Among case patient identifiable risk exposures, farm related (13.4%), recreational water related (8.1%), and unpasteurized milk/dairy product (7.0%) exposures were the most frequently noted. Relatively few infections involved raw/undercooked ground beef consumption (5.8%). Recent use of pulsed-field gel electrophoresis has facilitated linkage of sporadically reported cases into recognized outbreaks. E. coli O157:H7 infections frequently occur in Wisconsin; acquisition of these infections in a wide variety of settings poses important challenges to their prevention and control.
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