Abstract
Shiga toxin-producing Escherichia coli (STEC) may cause haemolytic uraemic syndrome (HUS). Age ≤5 years and presence of stx2a and eae are risk factors for the development of HUS. In this study, we investigated STEC isolates for the presence of adhesins, toxins and molecular risk assessment (MRA) factors to identify virulence genes associated with HUS development. We included non-duplicate isolates from all STEC infections (n = 340, HUS = 32) reported to the Norwegian National Reference Laboratory (NRL) for Enteropathogenic Bacteria from 1992 to 2013. The most common STEC were O157:H7/H− (34%) and O103:H2 (14%). We retrospectively screened the isolates by three multiplex polymerase chain reactions (PCRs) for adhesins (n = 11), toxins (n = 5) and MRA (n = 15). We calculated odds ratios (ORs) and adjusted odds ratios (aORs) for associations with HUS development. On average, isolates were positive for 15 virulence genes (range: 1–24); two toxins (range: 0–4), five adhesins (range: 0–8) and eight MRA genes (range: 0–13). The gene combinations were clustered within serotypes. Isolates from HUS cases were positive for eae and IpfAO26, and negative for saa, eibG, astA, cnf, subA and pic. We identified 11 virulence genes with a significant association to HUS development. Multivariable analyses adjusted for age group and Shiga toxin identified nleH1–2 [aOR 8.4, 95% confidence interval (CI); 2.18–32.3] as an independent risk factor for the development of HUS from an STEC infection. This study demonstrated that the non-LEE effector protein nleH1–2 may be an important predictor for elevated risk of developing HUS from STEC infections. We recommend the NRL for Enteropathogenic Bacteria to consider including nleH1–2 screening as part of routine STEC surveillance.
Highlights
Shiga toxin-producing Escherichia coli (STEC) is a zoonotic food- and waterborne pathogen of a serious public health concern because of its propensity to cause outbreaks, haemorrhagic colitis and the potentially life-threatening complication haemolytic uraemic syndrome (HUS) [1, 2]
In Norway, these associations were confirmed in a recent study which estimated the odds of developing HUS to be 16 times greater for children aged 5 years or less and 30 times greater for infections with stx2a-producing STEC [5]
We investigated the presence of 31 different virulence genes; five toxin genes, 12 adhesion genes and 14 molecular risk assessment (MRA)-associated genes, in addition to eae, ehxA and subtypes of stx1 and stx2, and their association with HUS development
Summary
Shiga toxin-producing Escherichia coli (STEC) is a zoonotic food- and waterborne pathogen of a serious public health concern because of its propensity to cause outbreaks, haemorrhagic colitis and the potentially life-threatening complication haemolytic uraemic syndrome (HUS) [1, 2]. It is estimated that 6–25% of patients infected with STEC develop HUS, with up to 50% requiring renal dialysis. In children, this rate is much higher [1]. HUS generally complicates 6–9% of STEC infections overall and about 15% of infections in children, with mortality of 2–5% and up to 30% developing longterm sequelae [2, 3]. The production of bacteriophage-encoded Shiga toxin 2a (Stx2a) by STEC is the primary virulence trait responsible for HUS development, along with the presence of intimin (eae) and young age of the host (≤5 years old) [4,5,6]. The clinical significance of STEC for humans is further determined by the production and interplay of
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