Low age (≤5 years), and Shiga toxin-producing E. coli (STEC) with stx2a and eae were identified as risk factors for HUS development.
However, not all patients with the above three risk factors developed HUS, meaning other strain characteristics or host specific factors, like the patient’s immune-competence, are also important when assessing risk.
Need to grade risk
STEC infection can lead to mild, self-limiting diarrhoea, haemorrhagic colitis or the life threatening complication HUS.
However, only a subgroup of STEC leads to HUS so identification of determinants differentiating high risk STEC (HUS STEC) from low risk STEC (non-HUS STEC) is needed to enable graded infectious disease response, said the researchers.
Outbreaks included one linked to cured sausage which sickened 17 people, 10 with HUS, in 2006 and another from lettuce which led to four illnesses, one with HUS, in 1999.
A national study of 333 STEC infections in Norway, including one STEC from each patient or outbreak over two decades (1992–2012), compared studies from other countries and contributed to understanding of the infection.
Serotype, virulence profile, and genotype of each STEC were determined by phenotypic or PCR based methods.
From 1992 through 2012, an increased number of STEC cases including more domestically acquired infections were notified in Norway.
From 1992 to 2006, 0–20 STEC cases were notified each year but from 2006, cases increased, ranging from 22 to 111 annually.
Of the 513 patients recorded by surveillance, 57 developed HUS.
Of the 333 patients selected for the study 25 developed HUS and yielded STEC with stx2, eae, and ehxA.
O157 was the most frequent serogroup (33.6%), although a decrease was seen over the last decade.
Compared to non-O157, O157 infection was significantly associated with older age, foreign travel prior to disease onset, and a higher rate of hospitalization, said the researchers.
Seven serogroups were found among STEC from HUS patients: O157 (including NSF O157 and SF O157 isolates), O145, O26, O103, O121, O111, and O86, however only serogroups SF O157 and O145 were significantly associated with HUS.
All HUS patients carried STEC with stx2, eae, and ehxA, however only stx2 and eae were significantly associated.
An association between the Shiga Toxin-encoding gene stx2, particularly the subtypes stx2a, stx2c, and stx2d, and development of HUS has previously been described, said the researchers.
Several other virulence factors that contribute to the pathogenicity of STEC have been identified, such as eae (E. coli attaching and effacing) encoding intimin and the plasmid-borne ehxA encoding enterohaemolysin.
The main aim was to identify microbiologic and patient-related criteria differentiating HUS STEC from non-HUS STEC, to get information enabling revision of control and prevention measures in Norway.
STEC infection was mandatory notifiable to the Norwegian Surveillance System for Communicable Diseases (MSIS) from 1995 and in 2006 diarrhoea-associated HUS became notifiable.
In Norway infections with non-O157 STEC were more common than infections with O157 isolates.
Researchers did not find any significant difference between STEC O157 and non-O157 regarding HUS.
Source: BMC Infectious Diseases 2015, 15:324
Online ahead of print, DOI: 10.1186/s12879-015-1017-6
“Shiga toxin-producing escherichia coli infections in Norway, 1992–2012: characterization of isolates and identification of risk factors for haemolytic uremic syndrome”
Authors: Lin T. Brandal, Astrid L. Wester, Heidi Lange, Inger Løbersli, Bjørn-Arne Lindstedt, Line Vold and Georg Kapperud