Distribution of class 1 integrons in historic and contemporary collections of human pathogenic Escherichia coli.

Integrons play a major role in the evolution and spread of antimicrobial resistance in human pathogens, including Escherichia coli. This study describes the occurrence of class 1 integrons in human pathogenic E. coli, in three isolate collections involving three periods from the last 100 years (i) the Murray collection (n = 58 bacteria isolated from the 1910s to 1940s); (ii) the E. coli reference (ECOR) collection (n = 37 isolates mainly from the 1980s); and (iii) a recently assembled collection (n = 88 isolates obtained in 2016). High-quality whole genome sequences (WGSs) were available for all isolates. Integrons were detected in the WGSs with the program IntegronFinder and the results compared with three established methods: (i) polymerase chain reaction detection of the integrase gene; (ii) BLAST searching using draft genomes; and (iii) mapping of short reads. No integrons were found in any of the Murray Collection isolates; however, integrons were present in 3% of the isolates from ECOR collection, assembled in the 1980s, and 26% of the isolates from the 2010s. Similarly, antimicrobial resistance determinants were not present in the Murray Collection isolates, whereas they were present in 19% of the ECOR Collection isolates and in 55% of the isolates obtained in during the 2010s.

Pneumonia-Specific Escherichia coli with Distinct Phylogenetic and Virulence Profiles, France, 2012-2014.

In a prospective, nationwide study in France of Escherichia coli responsible for pneumonia in patients receiving mechanical ventilation, we determined E. coli antimicrobial susceptibility, phylotype, O-type, and virulence factor gene content. We compared 260 isolates with those of 2 published collections containing commensal and bacteremia isolates. The preponderant phylogenetic group was B2 (59.6%), and the predominant sequence type complex (STc) was STc73. STc127 and STc141 were overrepresented and STc95 underrepresented in pneumonia isolates compared with bacteremia isolates. Pneumonia isolates carried higher proportions of virulence genes sfa/foc, papGIII, hlyC, cnf1, and iroN compared with bacteremia isolates. Virulence factor gene content and antimicrobial drug resistance were higher in pneumonia than in commensal isolates. Genomic and phylogenetic characteristics of E. coli pneumonia isolates from critically ill patients indicate that they belong to the extraintestinal pathogenic E. coli pathovar but have distinguishable lung-specific traits.

Locally Acquired mcr-1 in Escherichia coli, Australia, 2011 and 2013.

We identified discrete importation events of the mcr-1 gene on incompatibility group IncI2 plasmids in Escherichia coli isolated from patients in New South Wales, Australia, in 2011 and 2013. mcr-1 is present in a small minority of colistin-resistant Enterobacteriaceae and appears not to be established locally.

Secondary Shiga Toxin-Producing Escherichia coli Infection, Japan, 2010-2012.

To evaluate the potential public health risk caused by secondary Shiga toxin-producing Escherichia coli (STEC) infections in Japan, we investigated the prevalence and characteristics of STEC isolated from healthy adults during 2010-2012. Although prevalence among healthy adults was high, most STEC organisms displayed characteristics rarely found in isolates from symptomatic patients.

Food Source Prediction of Shiga Toxin-Producing Escherichia coli Outbreaks Using Demographic and Outbreak Characteristics, United States, 1998-2014.

BACKGROUND: Foodborne illness is a continuing public health problem in the United States. Although outbreak-associated illnesses represent a fraction of all foodborne illnesses, foodborne outbreak investigations provide critical information on the pathogens, foods, and food-pathogen pairs causing illness. Therefore, identification of a food source in an outbreak investigation is key to impacting food safety. OBJECTIVE: The objective of this study was to systematically identify outbreak-associated case demographic and outbreak characteristics that are predictive of food sources using Shiga toxin-producing Escherichia coli (STEC) outbreaks reported to Centers for Disease Control and Prevention (CDC) from 1998 to 2014 with a single ingredient identified. MATERIALS AND METHODS: Differences between STEC food sources by all candidate predictors were assessed univariately. Multinomial logistic regression was used to build a prediction model, which was internally validated using a split-sample approach. RESULTS: There were 206 single-ingredient STEC outbreaks reported to CDC, including 125 (61%) beef outbreaks, 30 (14%) dairy outbreaks, and 51 (25%) vegetable outbreaks. The model differentiated food sources, with an overall sensitivity of 80% in the derivation set and 61% in the validation set. CONCLUSIONS: This study demonstrates the feasibility for a tool for public health professionals to rule out food sources during hypothesis generation in foodborne outbreak investigation and to improve efficiency while complementing existing methods.

Summary of 11 years of enteric outbreak investigations and criteria to initiate an investigation, Province of Quebec, 2002 through 2012.

This article presents a retrospective analysis of enteric disease outbreak investigations led by or conducted in collaboration with provincial health authorities in the Province of Quebec from 2002 through 2012. Objectives were to characterize enteric disease outbreaks, quantify and describe those for which a source was identified (including the control measures implemented), identify factors that contributed to or impeded identification of the source, and recommend areas for improvement in outbreak investigations (including establishment of criteria to initiate investigations). A descriptive analysis of enteric disease outbreak summaries recorded in a provincial database since 2002 was conducted, and corresponding outbreak reports were reviewed. Among 61 enteric disease outbreaks investigated, primary pathogens involved were Salmonella (46%), Escherichia coli O157:H7 (25%), and Listeria monocytogenes (13%). Sources were identified for 37 (61%) of 61 of the outbreaks, and descriptive studies were sufficient to identify the source for 26 (70%) of these. During the descriptive phase of the investigation, the causes of 21 (81%) of 26 outbreaks were identified by promptly collecting samples of suspected foods based on case interviews. Causes of outbreaks were more likely to be detected by weekly surveillance or alert systems (odds ratio = 6.0, P = 0.04) than by serotyping or molecular typing surveillance and were more likely to be associated with a common event or location (odds ratio = 11.0, P = 0.023). Among the 37 outbreaks for which causes were identified, 24 (65%) were associated with contaminated food, and recalls were the primary control measure implemented (54%). Review of enteric outbreaks investigated at the provincial level in Québec has increased the province's ability to quantify success and identify factors that can promote success. Multiple criteria should be taken into account to identify case clusters that are more likely to be resolved.

Overview and Historical Perspectives.

In this overview, we describe the history of Shiga toxin (Stx)-producing Escherichia coli (STEC) in two phases. In phase one, between 1977 and 2011, we learned that E. coli could produce Shiga toxin and cause both hemorrhagic colitis and the hemolytic-uremic syndrome in humans and that the prototype STEC-E. coli O157:H7-adheres to and effaces intestinal epithelial cells by a mechanism similar to that of enteropathogenic E. coli. We also recognized that the genes for Stx are typically encoded on a lysogenic phage; that STEC O157:H7 harbors a large pathogenicity island that encodes the elements needed for the characteristic attaching and effacing lesion; and that the most severe cases of human disease are linked to production of Stx type 2a, not Stx type 1a. Phase two began with a large food-borne outbreak of hemorrhagic colitis and hemolytic-uremic syndrome in Germany in 2011. That outbreak was caused by a novel strain consisting of enteroaggregative E. coli O104:H4 transduced by a Stx2a-converting phage. From this outbreak we learned that any E. coli strain that can adhere tightly to the human bowel (either by a biofilm-like mechanism as in E. coli O104:H4 or by an attaching and effacing mechanism as in E. coli O157:H7) can cause severe diarrheal and systemic illness when it acquires the capacity to produce Stx2a. This overview provides the basis for the review of current information regarding these fascinating and complex pathogens.

The Canadian contribution to the science of verotoxigenic Escherichia coli and associated illnesses: the early years.

As stories of microbiological and infectious disease discoveries are told, one of the most charming of these in Canadian history is the recognition of verotoxigenic Escherichia coli (VTEC) and associated disease. The considerable burden and impact of VTEC-associated infections is currently experienced worldwide. Jack Konowalchuk, Joan Speirs, and their collaborators in Ottawa, Ontario, defined the E. coli verotoxin. Mohamed Karmali, Martin Petric, and colleagues at The Hospital for Sick Children in Toronto, Ontario, established the association of VTEC and hemolytic-uremic syndrome. Nationwide, and with the dissemination of knowledge through the central health directorate in Ottawa, numerous scientists and clinicians were motivated to focus on this theme, and within a relatively brief chronology, much became known about the biology of VTEC and the pathogenesis, epidemiology, and clinical aspects of disease. Many Canadian investigators, but especially those in the veterinary school at Guelph, Ontario, also contributed to the science of VTEC among animals. The interactions between clinical and veterinary researchers led to a then unprecedented exponential growth in the knowledge base of VTEC. Canadians also participated in a better understanding of the origin and potential of the E. coli O157 serogroup. Whereas not exclusively Canadian, the contributions of our national scientists in this field must be seen as a vital part of medical and microbiological Canadiana; this essence is captured in this historical review.

Molecular epidemiology of extended-spectrum ß-lactamase-, AmpC ß-lactamase- and carbapenemase-producing Escherichia coli and Klebsiella pneumoniae isolated from Canadian hospitals over a 5 year period: CANWARD 2007-11.

OBJECTIVES: To assess the proportion of Escherichia coli and Klebsiella pneumoniae from Canadian hospitals that produce extended-spectrum ß-lactamases (ESBLs), AmpC ß-lactamases and carbapenemases, as well as to describe the patterns of antibiotic resistance and molecular characteristics of these organisms. METHODS: Some 5451 E. coli and 1659 K. pneumoniae were collected from 2007 to 2011 inclusive as part of the ongoing CANWARD national surveillance study. Antimicrobial susceptibility testing was performed to detect putative ESBL, AmpC and carbapenemase producers, which were then further characterized by PCR and sequencing to detect resistance genes. In addition, isolates were characterized by PFGE and an allele-specific PCR to detect isolates of sequence type (ST) 131. RESULTS: The proportion of ESBL-producing E. coli (2007, 3.4%; 2011, 7.1%), AmpC-producing E. coli (2007, 0.7%; 2011, 2.9%) and ESBL-producing K. pneumoniae (2007, 1.5%; 2011, 4.0%) among the isolates collected increased during the study period. The majority of ESBL-producing E. coli (>95%), AmpC-producing E. coli (>97%) and ESBL-producing K. pneumoniae (>89%) remained susceptible to colistin, amikacin, ertapenem and meropenem. Isolates were generally unrelated by PFGE (<80% similarity); however, ST131 was identified among 55.8% and 28.7% (P < 0.001) of ESBL- and AmpC-producing E. coli, respectively. CTX-M-15 was the dominant genotype in both ESBL-producing E. coli (66.2%) and ESBL-producing K. pneumoniae (50.0%), while the dominant genotype in AmpC-producing E. coli was CMY-2 (55.7%). Carbapenemase production was identified in 0.04% (n = 2) of E. coli and 0.06% (n = 1) of K. pneumoniae, all of which produced KPC-3. CONCLUSIONS: The proportion of ESBL- and AmpC-producing E. coli and K. pneumoniae increased significantly during the study period, while the number of carbapenemase producers remained low (<1%). Compared with AmpC-producing E. coli, ESBL-producing E. coli were significantly associated with multidrug resistance and the ST131 clone.

[The Austrian pediatrician Theodor Escherich as bacteriologist and social hygienist: The 100th anniversary of his death on February 15th, 1911]. / Der österreichische Pädiater Theodor Escherich als Bakteriologe und Sozialhygieniker: Zur 100. Wiederkehr seines Todestages am 15. Feber 1911.

Escherich was born on November 29, 1857 in Ansbach, Bavaria. He has been director of the children hospitals in Graz (Styria, Austria) from 1890 and Vienna (Austria) from 1902, started his bacteriological investigations in 1884 during a short stay in St. Anna Children Hospital in Vienna. This he continued it as an assistant in Munich and as clinic director in Graz. On the basis of his bacteriological findings in breast-milk, which proved to be sterile, he wanted to detect the physiological and pathogenetic role of the intestinal flora of breast-fed babies and of infants. In stained slides of meconium and milk-faeces he found cocci, bacilli with and without spores and yeasts. Among them he intensively investigated both the "Bacterium lactis aërogenes" (now: "Aerobacter aerogenes"), and the "Bacterium coli commune". In 1919, 8 years after his death, the name "Escherichia coli" was used for the first time and became the valid species name. This posthumous honour made Escherich worldwide known in the medical profession. Also for further enteric pathogens, the Campylobacter/Helicobacter group, which could not be cultured in Escherich's time he is looked upon as the first describer. In Graz and particularly in Vienna, Escherich's social-medical activities were concentrated on the baby and infant welfare. This was promoted by the construction of baby departments in hospitals, instructions of mothers, improvement of baby nutriments, and training of baby nurses and midwifes. The first great aim was the establishment of the "Reichsanstalt für Mutter- und Säuglingsfürsorge" (Imperial Institution for Mother and Baby Welfare) in Vienna which could come in action only during World War I in October 1915, thus 4 1/2 years after Escherich's death on February 15, 1911.

Therapy for and prevention of traveler's diarrhea.

Acute diarrhea associated with international travel is commonly caused by enterotoxigenic Escherichia coli, enteroaggregative E. coli, or noroviruses. Early studies to define these enteropathogens took place at the University of Maryland during the Theodore E. Woodward years. Although a reduction in the rate of diarrhea may be possible through avoidance of foods and beverages likely to be contaminated, a more effective preventive strategy is to administer nonabsorbed (<0.4%) rifaximin each day during trips to areas where the risk of traveler's diarrhea is high (i.e., high-risk areas). For the self-treatment of diarrhea that occurs during travel, all persons planning trips to high-risk areas should take with them medication with expected activity against the prevalent bacterial enteropathogens: rifaximin (for the treatment of common afebrile, nondysenteric diarrhea), a fluoroquinolone, or azithromycin. Further study is needed to determine whether it is possible to avoid important morbidity associated with diarrhea and the development of postinfectious irritable bowel syndrome with chemoprophylaxis and/or early effective treatment.

Enterotoxigenic Escherichia coli in developing countries: epidemiology, microbiology, clinical features, treatment, and prevention.

ETEC is an underrecognized but extremely important cause of diarrhea in the developing world where there is inadequate clean water and poor sanitation. It is the most frequent bacterial cause of diarrhea in children and adults living in these areas and also the most common cause of traveler's diarrhea. ETEC diarrhea is most frequently seen in children, suggesting that a protective immune response occurs with age. The pathogenesis of ETEC-induced diarrhea is similar to that of cholera and includes the production of enterotoxins and colonization factors. The clinical symptoms of ETEC infection can range from mild diarrhea to a severe cholera-like syndrome. The effective treatment of ETEC diarrhea by rehydration is similar to treatment for cholera, but antibiotics are not used routinely for treatment except in traveler's diarrhea. The frequency and characterization of ETEC on a worldwide scale are inadequate because of the difficulty in recognizing the organisms; no simple diagnostic tests are presently available. Protection strategies, as for other enteric infections, include improvements in hygiene and development of effective vaccines. Increases in antimicrobial resistance will dictate the drugs used for the treatment of traveler's diarrhea. Efforts need to be made to improve our understanding of the worldwide importance of ETEC.