Investigation of an Escherichia coli O145 outbreak in a child day-care centre - extensive sampling and characterization of eae- and stx 1-positive E. coli yields epidemiological and socioeconomic insight

Abstract

BackgroundOn October 29th 2009 the health authorities in the city of Trondheim, Norway were alerted about a case of Shiga toxin-positive E. coli (STEC) O145 in a child with bloody diarrhoea attending a day-care centre. Symptomatic children in this day-care centre were sampled, thereby identifying three more cases. This initiated an outbreak investigation.MethodsA case was defined as a child attending the day-care centre, in whom eae- and stx1- but not stx2-positive E. coli O145:H28 was diagnosed from a faecal sample, with multilocus variable number of tandem repeat analysis (MLVA) profile identical to the index isolate. All 61 children, a staff of 14 in the day-care centre, and 74 close contacts submitted faecal samples. Staff and parents were interviewed about cases' exposure to foods and animals. Faecal samples from 31 ewes from a sheep herd to which the children were exposed were analyzed for E. coli O145.ResultsSixteen cases were identified, from which nine presented diarrhoea but not haemolytic uremic syndrome (HUS). The attack rate was 0.26, and varied between age groups (0.13-0.40) and between the three day-care centre departments (0.20-0.50), and was significantly higher amongst the youngest children. Median duration of shedding was 20 days (0-71 days). Children were excluded from the day-care centre during shedding, requiring parents to take compassionate leave, estimated to be a minimum total of 406 days for all cases. Atypical enteropathogenic E. coli (aEPEC) were detected among 14 children other than cases. These isolates were genotypically different from the outbreak strain. Children in the day-care centre were exposed to faecal pollution from a sheep herd, but E. coli O145 was not detected in the sheep.ConclusionsWe report an outbreak of stx1- and eae-positive STEC O145:H28 infection with mild symptoms among children in a day-care centre. Extensive sampling showed occurrence of the outbreak strain as well as other STEC and aEPEC strains in the outbreak population. MLVA-typing of the STEC-isolates strongly indicates a common source of infection. The study describes epidemiological aspects and socioeconomic consequences of a non-O157 STEC outbreak, which are less commonly reported than O157 outbreaks.

PCR-Based Detection and Molecular Characterization of Shiga Toxin-Producing Escherichia coli Strains in a Routine Microbiology Laboratory over 16 years

“…The largest local outbreak occurred in a kindergarten in 2009 where 15 isolates of STEC serotype O145:H28 were of the same MLVA genotype. Although the index child presented with bloody diarrhea, none of the children affected in that outbreak developed HUS (49).…”

The epidemiology, microbiology and clinical impact of Shiga toxin-producingEscherichia coliin England, 2009–2012

“…Transmission to humans occurs through either consumption of contaminated food or water, or exposure to a contaminated environment involving direct or indirect contact with animals or their faeces [2,3]. While small outbreaks due to person-to-person spread are reported in closed settings, particularly childcare facilities [7,8], large outbreaks are often associated with foodborne transmission [9,10], and contact with ruminants, such as in open farms [11,12]. STEC cause both sporadic and epidemic infections.…”

Evolution of Enterohemorrhagic Escherichia coli O26 Based on Single-Nucleotide Polymorphisms

“…In humans, EHEC infections cause watery and bloody diarrhea, hemolytic uremic syndrome (HUS) (Tarr et al 2005; Mellmann et al 2009), and is the most common cause of acute renal failure in children (Brandt et al 1994; Kaplan 1998; Tarr et al 2005). Although EHEC O157:H7 is the serotype most commonly associated with HUS worldwide (Banatvala et al 2001; Robert-Koch-Institut 2008; Centers for Disease Control and Prevention [CDC] 2011), the large O104:H4 outbreak in Germany in spring 2011 (Bielaszewska et al 2011; Mellmann et al 2011) and several outbreaks caused by other non-O157 EHEC such as O26 (Bradley et al 2012; Brown et al 2012; L’Abée-Lund et al 2012; Wahl et al 2011) attest to the potential menace of non-O157 EHEC. Among these, EHEC O26:H11/H − (nonmotile) are the serotypes that are most frequently associated with severe human diseases in Europe (Gerber et al 2002; Tozzi et al 2003; Ethelberg et al 2004; Espié et al 2008; Mellmann et al 2008; Zimmerhackl et al 2010; Käppeli et al 2011; Buvens et al 2012) and the United States (Jelacic et al 2003; Brooks et al 2005; Hedican et al 2009).…”