Verotoxigenic E. coli (VTEC) is the cause of severe gastrointestinal infection especially among infants. Between 10 and 20 cases are reported annually to the National Infectious Disease Register (NIDR) in Finland. The aim of this study was to identify explanatory variables for VTEC infections reported to the NIDR in Finland between 1997 and 2006. We applied a hurdle model, applicable for a dataset with an excess of zeros.
We enrolled 131 domestically acquired primary cases of VTEC between 1997 and 2006 from routine surveillance data. The isolated strains were characterized by virulence type, serogroup, phage type and pulsed-field gel electrophoresis. By applying a two-part Bayesian hurdle model to infectious disease surveillance data, we were able to create a model in which the covariates were associated with the probability for occurrence of the cases in the logistic regression part and the magnitude of covariate changes in the Poisson regression part if cases do occur. The model also included spatial correlations between neighbouring municipalities.
The average annual incidence rate was 4.8 cases per million inhabitants based on the cases as reported to the NIDR. Of the 131 cases, 74 VTEC O157 and 58 non-O157 strains were isolated (one person had dual infections). The number of bulls per human population and the proportion of the population with a higher education were associated with an increased occurrence and incidence of human VTEC infections in 70 (17%) of 416 of Finnish municipalities. In addition, the proportion of fresh water per area, the proportion of cultivated land per area and the proportion of low income households with children were associated with increased incidence of VTEC infections.
With hurdle models we were able to distinguish between risk factors for the occurrence of the disease and the incidence of the disease for data characterised by an excess of zeros. The density of bulls and the proportion of the population with higher education were significant both for occurrence and incidence, while the proportion of fresh water, cultivated land, and the proportion of low income households with children were significant for the incidence of the disease.
This report describes a study carried out to gain baseline information on the molecular characteristics of extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli and Klebsiella spp. in Canada. A total of 29,323 E. coli and 5,156 Klebsiella sp. isolates were screened at 12 participating sites. Of these, 505 clinically significant, nonrepeat isolates displaying reduced susceptibility to the NCCLS-recommended beta-lactams were submitted to a central laboratory over a 1-year period ending on 30 September 2000. A total of 116 isolates were confirmed to be ESBL producers. PCR and sequence analysis revealed the presence of TEM-11 (n = 1), TEM-12 (n = 1), TEM-29 (n = 1), TEM-52 (n = 4), CTX-M-13 (n = 1), CTX-M-14 (n = 15), CTX-M-15 (n = 11), SHV-2 (n = 2), SHV-2a (n = 12), SHV-5 (n = 6), SHV-12 (n = 45), and SHV-30 (n = 2). Five novel beta-lactamases were identified and designated TEM-115 (n = 2), TEM-120 (n = 1), SHV-40 (n = 2), SHV-41 (n = 4), and SHV-42 (n = 1). In addition, no molecular mechanism was identified for five isolates displaying an ESBL phenotype. Macrorestriction analysis of all ESBL isolates was conducted, as was restriction fragment length polymorphism analysis of plasmids harboring ESBLs. Although a "clonal" distribution of isolates was observed at some individual sites, there was very little evidence suggesting intrahospital spread. In addition, examples of identical or closely related plasmids that were identified at geographically distinct sites across Canada are given. However, there was considerable diversity with respect to plasmid types observed.
Rapid bacterial typing is a valuable and necessary tool in the prevention and detection of outbreaks. The purpose of this study was to adapt a multilocus variable number of tandem repeats analysis (MLVA) for analysis on a benchtop capillary electrophoresis instrument and compare the modified assay with multilocus sequence typing (MLST) for typing cefpodoxime-resistant Escherichia coli (E. coli). Further, we identified the causative resistance mechanisms and epidemiological type of infection for isolates producing extended-spectrum ß-lactamases (ESBLs). A collection of E. coli resistant to cefpodoxime was typed by MLST and a modified MLVA assay using a benchtop capillary electrophoresis instrument. Resistance mechanisms were identified by polymerase chain reaction (PCR) and sequencing. Patient history was examined to establish the epidemiological type of infection for ESBL-producing E. coli. MLVA yielded typing results homologous with MLST and it correctly identified E. coli sequence type (ST) 131 that was accounting for 45 % of all ESBL-producing isolates in the sample collection. The majority (76.7 %) of ESBL-producing isolates was healthcare-related and only 23.3 % of the ESBL-producing isolates were community-onset infections (COI), regardless of the ST. Patients with COI were significantly more often of female gender and younger age compared to healthcare-associated infections (HCAI) and hospital-onset infections (HOI). In conclusion, the modified MLVA is a useful tool for the rapid typing of E. coli and it identified ST131 as the predominating ESBL-producing lineage in Copenhagen. Healthcare-related infections were the predominant infection setting of ESBL-producing E. coli and the demographic characteristics differed between patients with COI and healthcare-related infections.
In spring 2009 in Adler colony of the Institute of Medical Primatology, a large enzootic outbreak of acute intestine infection associated with pathogenic E. coli occurred and caused 5% mortality of population (209 animals).
The epidemiological analysis, bacteriological investigation, postmortem examination, histological analysis, and PCR were used to identify the infectious agent.
Marked hemorrhagic diathesis, lethargy, dehydration, diarrhea with blood, wasting, and sometimes dystrophic changes in articular cartilages were noted. Morphologically, hemorrhagic enterocolitis and massive hemorrhages were found. PCR investigation of bacteriologically isolated E. coli characterized it as enteropathogenic and enteroinvasive E. coli.
The outbreak in Adler colony slightly differed from similar outbreak in Florida in 2014 by more marked hemorrhagic diathesis and articular changes in some monkeys caused by polyavitaminosis developed in the course of infection. Sensitive to infection were M. mulatta, M. fascicularis, Cercopithecus aethiops, P. hamadryas and anubis, and Cebus capucinus.
Acute bacterial gastroenteritis is associated with subsequent post-infectious irritable bowel syndrome (PI-IBS) in adults. Less is known about this relationship in children. In May 2000, contamination of municipal water by Escherichia coli 0157:H7 and Campylobacter species caused a large outbreak of acute gastroenteritis in Walkerton, Ontario. We assessed this association among a cohort of children enrolled in the Walkerton Health Study (WHS).
WHS participants who were under age 16 at the time of the outbreak but who reached age 16 during the 8-year study follow-up were eligible for the pediatric PI-IBS study cohort. Eligibility also required no diagnosis of IBS or inflammatory bowel disease before the outbreak and permanent residency in the Walkerton postal code at the time of the outbreak. Validated criteria were used to classify subjects as having had no gastroenteritis (unexposed controls), self-reported gastroenteritis, or clinically suspected gastroenteritis during the outbreak. From 2002 to 2008, standardized biennial interviews used a modified Bowel Disease Questionnaire to diagnose IBS by Rome I criteria. Risk factors for IBS were identified by logistic regression.
In all, 467 subjects were eligible for the pediatric PI-IBS study cohort (47.1% female; mean age 11.6+/-2.44 years at the time of the outbreak). Of these, 305 were exposed to GE (130 clinically suspected and 175 self-reported) and 162 were unexposed controls. The cumulative incidence of IBS was significantly increased among exposed subjects vs. controls (10.5% vs. 2.5%; odds ratio 4.6, 95% confidence interval (1.6, 13.3)). In an unadjusted risk factor analysis, IBS was associated with a shorter time interval from exposure to assessment of IBS symptoms, female gender, diarrheal illness lasting more than 7 days, weight loss >10 lb, and antibiotic use during the outbreak. In adjusted analyses, both female gender and time interval to assessment of IBS symptoms remained independent predictors of PI-IBS.
Acute bacterial gastroenteritis is associated with subsequent IBS in children as in adults. Risk factors for PI-IBS in children are similar to those identified among adults. Confirmation of these findings in similar cohorts is needed.
In the summer of 1991 a large outbreak of Escherichia coli O157:H7 associated diarrhea occurred in 6 Inuit communities in the Canadian Northwest Territories. The total population of these communities is 5,292. Of the 521 individuals who developed diarrhea, 152 (29%) were positive for E. coli O157:H7 on stool culture or positive by verotoxin analysis. Median age was 6 years. The attack rate for children
A cluster of E. coli O157:H7 hemorrhagic colitis was identified in metro Edmonton, Alberta through notifiable disease surveillance in late 2002.
Environmental health officers collected food histories and clinical information from cases in the cluster. The provincial public health laboratory conducted pulsed field gel electrophoresis (PFGE) analysis on E. coli O157:H7 isolates from cluster cases. Public health and food regulatory agencies conducted an investigation when a food source (unpasteurized gouda cheese) was implicated.
PFGE analysis revealed an "outbreak" profile in 13 cases. Onset dates for the outbreak cases ranged between October 2002 and February 2003. Two cases, aged 22 months and 4 years, developed hemolytic uremic syndrome as a result of their infection. Consumption of unpasteurized gouda cheese produced at a local dairy farm was reported by 12 of 13 outbreak cases in the 2 to 8 days prior to illness. E. coli O157:H7 was isolated from 2 of 26 cheese samples manufactured by the implicated producer. The cheese isolates had indistinguishable PFGE profiles as compared with outbreak case isolates. Implicated cheese was found to be contaminated with E. coli O157:H7 104 days after production, despite having met regulated microbiological and aging requirements.
To our knowledge, this is the first confirmed outbreak of E. coli O157:H7 infection in Canada associated with raw milk hard cheese. A review of federal legislation vis-à-vis raw milk hard cheese may be in order.
During the spring of 2006, a national disease outbreak caused by Shiga toxin-producing Escherichia coli (STEC) O103:H25 was investigated in Norway. At the time of the outbreak the Norwegian School of Veterinary Science was the national reference laboratory for E. coli O157 in food, and the microbiological investigations to identify the food source were performed there. Food- and environmental samples (n=931) were collected by the Norwegian Food Safety Authorities following two different hypotheses i) that minced meat was the source of STEC, and ii) that fermented sausage was the source of STEC. Twenty seven food samples, all collected following the latter hypothesis contained eae-positive E. coli O103:H25, but none of these were stx-positive. By PFGE it was shown that isolates from one particular type of fermented sausage "morr sausage 1" were identical to the isolates from patients. Samples of sheep meat that were linked epidemiologically to meat used for sausage production also contained isolates identical or closely related to patient strains. The presented study underpins epidemiological indications that fermented sausage was the source of the outbreak, but points specifically to one particular brand of sausage as the source.