Epidemiology of Shiga toxin producing Escherichia coli in Australia, 2000-2010 (original) (raw)
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Emerging Infectious Diseases, 2017
During a large outbreak of Shiga toxin−producing Escherichia coli illness associated with an agricultural show in Australia, we used whole-genome sequencing to detect an IS1203v insertion in the Shiga toxin 2c subunit A gene of Shiga toxin−producing E. coli. Our study showed that clinical illness was mild, and hemolytic uremic syndrome was not detected. S higa toxin−producing Escherichia coli (STEC) is a major cause of serious human gastrointestinal illness and has the potential to cause life-threatening complications, such as hemolytic uremic syndrome (HUS) (1). An average of 0.4 cases of STEC illness per 100,000 persons per year are reported to public health authorities in Australia (2). Disease severity can range from asymptomatic infection to serious and sometimes fatal illness, particularly in young children and the elderly (3,4). Healthy ruminants, particularly cattle, are the reservoir for STEC (5). Human infection with STEC usually occurs as a result of inadvertent ingestion of fecal matter after consumption of contaminated food, water, or unpasteurized milk; contact with animals or their environments; or secondarily, through contact with infected humans (4,5). In the largest previously reported outbreak of STEC illness in Australia in 1995, which was associated with consumption of mettwurst (uncooked, semidry, fermented sausages), HUS developed in 23 of the 51 case-patients identified, and there was 1 death (6). The Study A multidisciplinary incident management team was established to investigate an outbreak of STEC illness associated with an annual agricultural show in Brisbane, Queensland, Australia, in August 2013 (online Technical Appendix, https://wwwnc.cdc.gov/EID/article/23/10/16-1836-Techapp1.pdf). The incident management team defined primary and secondary outbreak cases (online Technical Appendix). Persons with laboratory-confirmed STEC infection associated with the outbreak and their household contacts were followed up until the point of microbiological evidence of clearance, which was defined as 2 consecutive negative stool samples collected >24 h apart (7). Case-patients and contacts with a high risk for transmission (persons <5 years of age; persons unable to maintain good hygiene; or childcare, healthcare, aged care, or food preparation workers) were advised to avoid childcare and work settings in accordance with Queensland Health Guidelines (7). Enhanced surveillance measures were implemented to assist with case finding (online Technical Appendix). Medical practitioners were requested to avoid use of antimicrobial drugs for suspected case-patients with STEC infections because of previously reported associations between antimicrobial drug use and HUS (online Technical Appendix). We developed a case−control study to obtain additional information related to animal contact, hand hygiene, and food consumption at the agricultural show (online Technical Appendix). We analyzed data by using Epi Info 7 (Centers for Disease Control and Prevention, Atlanta, GA, USA) (online Technical Appendix). STEC identified from human, environmental, and animal samples were serotyped for O and H antigens (online Technical Appendix). Expression of Shiga toxin 1 (stx1) and stx2 genes was determined for selected isolates (online Technical Appendix). Shiga toxin gene subtyping and whole-genome sequencing (WGS) analysis was performed (online Technical Appendix). During August 21−September 27, 2013, we identified 57 outbreak-associated laboratory-confirmed case-patients with STEC infection: 54 confirmed primary case-patients, 1 probable primary case-patient, and 2 secondary case-patients (Figure 1). Of the 57 case-patients, 32 (56%) were
BMC Infectious Diseases, 2013
Background: Shiga toxin-producing Escherichia coli (STEC) O157:H7 and related non-O157 STEC strains are enteric pathogens of public health concern worldwide, causing life-threatening diseases. Cattle are considered the principal hosts and have been shown to be a source of infection for both foodborne and environmental outbreaks in humans. The aims of this study were to investigate risk factors associated with sporadic STEC infections in humans in New Zealand and to provide epidemiological information about the source and exposure pathways. Methods: During a national prospective case-control study from July 2011 to July 2012, any confirmed case of STEC infection notified to regional public health units, together with a random selection of controls intended to be representative of the national demography, were interviewed for risk factor evaluation. Isolates from each case were genotyped using pulsed-field gel electrophoresis (PFGE) and Shiga toxin-encoding bacteriophage insertion (SBI) typing.
Surveillance of Shiga toxigenic Escherichia coli in Australia
Communicable diseases intelligence quarterly report, 2005
All Australian States and Territories have low rates (< or = 0.32 cases per 100,000 population) of notification for Shiga toxin-producing Escherichia coli (STEC), except for South Australia where the rates are ten-fold higher at 2.58 cases per 100,000 population. To explore possible reasons for the variation in rates we surveyed public health reference laboratories to determine the methods used and number of specimens tested for these organisms. Only five of eight jurisdictions routinely conducted testing for STEC, and polymerase chain based tests were most common. Culture was also common and in one jurisdiction that tests specimens with culture, approximately 1.2 per cent of specimens were positive. The notification rates for different jurisdictions reflected the number of specimens tested, with jurisdiction testing < or = 500 specimens having rates < or = 0.32 cases per 100,000 population. The use of culture as a test method may also influence notification rates. Public h...
Clinical Microbiology and Infection, 2008
Detection of Shiga toxin-producing Escherichia coli (STEC) in The Netherlands is traditionally limited to serogroup O157. To assess the relative importance of STEC, including non-O157 serogroups, stool samples submitted nationwide for investigation of enteric pathogens or diarrhoea were screened with real-time PCR for the presence of the Shiga toxin genes. Patients were selected if their stool contained blood upon macroscopic examination, if they had a history of bloody diarrhoea, were diagnosed with haemolytic uraemic syndrome, or were aged <6 years (irrespective of the bloody aspect of the stool). PCR-positive stools were forwarded to a central laboratory for STEC isolation and typing. In total, 4069 stools were examined, with 68 (1.7%) positive PCR results. The highest prevalence was for stools containing macroscopic blood (3.5%), followed by stools from patients with a history of bloody diarrhoea (2.4%). Among young children, the prevalence (1.0%) was not significantly higher than among random, non-bloody, stool samples from diarrhoeal patients (1.4%). STEC strains were isolated from 25 (38%) PCR-positive stools. Eleven O-serogroups were detected, including five STEC O157 strains. As serogroup O157 represented only 20% of the STEC isolates, laboratories should be encouraged to use techniques enabling them to detect non-O157 serogroups, in parallel with culture, for isolation and subsequent characterisation of STEC strains for public health surveillance and detection of outbreaks.
Clinical Infectious Diseases, 2011
Background. The epidemiology over time of non-O157 Shiga toxin-producing Escherichia coli (STEC) is unknown. Since 1999, increasing numbers of laboratories in Connecticut have been testing for ST rather than culturing for O157, enabling identification of non-O157 STEC. Methods. Beginning in 2000, Connecticut laboratories were required to submit ST-positive broths to the State Laboratory for isolation and typing of STEC. The ratio of non-O157:O157 from laboratories conducting ST testing was used to determine state-level estimates for non-O157 STEC. Patients with STEC were interviewed for exposure factors in the 7 days preceding illness. Incidence trends, clinical features, and epidemiology of non-O157 and O157 STEC infections were compared. Results. From 1 January 2000 through 31 December 2009, ST testing detected 392 (59%) of 663 reported STEC infections; 229 (58%) of the isolates were non-O157. The estimated incidence of STEC infection decreased by 34%. O157 and the top 4 non-O157 serogroups, O111, O103, O26, and O45, were a stable percentage of all STEC isolates over the 10-year period. Bloody diarrhea, hospitalization, and hemolytic uremic syndrome were more common in patients with O157 STEC than in patients with non-O157 STEC infection. Exposure risks of patients with non-O157 STEC infection differed from those of patients with O157 STEC infection primarily in international travel (15.3% vs 2.5%; P , .01). Non-O157 types differed from each other with respect to several epidemiologic and exposure features. Conclusions. Both O157 and non-O157 STEC infection incidence decreased from 2000 through 2009. Although infection due to O157 is the most common and clinically severe STEC infection, it accounts for a minority of all clinically significant STEC infections. STEC appear to be a diverse group of organisms that have some differences as well as many epidemiologic and exposure features in common.
Emerging Infectious Diseases, 2021
O ver the previous decade, the Republic of Ireland has frequently reported the highest incidence rates of symptomatic Shiga toxin-producing Escherichia coli (STEC) infection in the European Union (EU) (1). The reported national crude incidence rate (CIR) of confi rmed STEC infections in Ireland during 2017 was 923 cases (16.6 cases/100,000 population), equating to ≈10 times the EU average (1.66 cases/100,000 population) (1,2). Shiga toxin-producing E. coli bacteria, of which there are >100 serotypes, were fi rst discovered in 1977; the most well-known STEC strain, E. coli O157:H7, was fi rst recognized as a pathogen in 1982. The Shiga toxin-producing group of E. coli includes serotypes O157, O26, and other enterohemorrhagic E. coli bacteria; serotypes are typically categorized by the presence of stx1 or stx2 genes (3). STEC is associated with a wide range of sequelae, from mild diarrhea to hemorrhagic colitis, hematochezia (bloody diarrhea), thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome (HUS) causing intravascular lysis of red blood cells (2,4). Infection is characterized by several transmission routes, including consumption of contaminated food and water, person-to-person contact, or direct contact with infected animals (4,5). A recent study found the incidence of confi rmed sporadic (i.e., nonoutbreak) STEC O157 infection in Ireland in 2008-2013 signifi cantly elevated in regions characterized by high reliance on private groundwater (odds ratio [OR] 18.727; p<0.001) and high livestock densities (OR 1.001; p = 0.007) (6). Transmission sources, pathways, and sourcepathway interactions associated with STEC infection in Ireland are multifaceted, resulting in a complex exposure profi le (7,8). Sporadic cases of infection are inherently diffi cult to attribute to specifi c risk factors for reasons that include the absence of accurate dateof-onset data, underreporting, misdiagnosis, myriad potential exposures, and surveillance limitations (5,6,7). Of 2,210 confi rmed STEC cases reported in Ireland during 2008-2013, a total of 1,264 (57.2%) were defi ned as sporadic (6). The high proportion of sporadic STEC infections relative to total annual cases in Ireland, and their association with environmental exposures, has made the spatiotemporal occurrence of STEC particularly important in public health. We used a suite of
BMC Microbiology, 2008
Background: Shiga toxin-producing Escherichia coli (STEC) is an important cause of bloody diarrhoea (BD), non-bloody diarrhoea (NBD) and the haemolytic uraemic syndrome (HUS). In Argentina and New Zealand, the most prevalent STEC serotype is O157:H7, which is responsible for the majority of HUS cases. In Australia, on the other hand, STEC O157:H7 is associated with a minority of HUS cases. The main aims of this study were to compare the phenotypic and genotypic characteristics of STEC O157 strains isolated between 1993 and 1996 from humans in Argentina, Australia and New Zealand, and to establish their clonal relatedness. Results: Seventy-three O157 STEC strains, isolated from HUS (n = 36), BD (n = 20), NBD (n = 10), or unspecified conditions (n = 7) in Argentina, Australia and New Zealand, were analysed. The strains were confirmed to be E. coli O157 by biochemical tests and serotyping. A multiplex polymerase chain reaction (PCR) was used to amplify the stx 1 , stx 2 and rfb O157 genes and a genotyping method based on PCR-RFLP was used to determine stx 1 and stx 2 variants. This analysis revealed that the most frequent stx genotypes were stx 2 /stx 2c (vh-a) (91%) in Argentina, stx 2 (89%) in New Zealand, and stx 1 /stx 2 (30%) in Australia. No stx 1-postive strains were identified in Argentina or New Zealand. All strains harboured the eae gene and 72 strains produced enterohaemolysin (EHEC-Hly). The clonal relatedness of strains was investigated by phage typing and pulsed-field gel electrophoresis (PFGE). The most frequent phage types (PT) identified in Argentinian, Australian, and New Zealand strains were PT49 (n = 12), PT14 (n = 9), and PT2 (n = 15), respectively. Forty-six different patterns were obtained by XbaI-PFGE; 37 strains were grouped in 10 clusters and 36 strains showed unique patterns. Most clusters could be further subdivided by BlnI-PFGE. Conclusion: STEC O157 strains isolated in Argentina, Australia, and New Zealand differed from each other in terms of stx-genotype and phage type. Additionally, no common PFGE patterns were found in strains isolated in the three countries. International collaborative studies of the type reported here are needed to detect and monitor potentially hypervirulent STEC clones.