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. 2017 Aug;36(8):1433-1441.
doi: 10.1007/s10096-017-2950-7. Epub 2017 Apr 19.

Genetic makeup of Shiga toxin-producing Escherichia coli in relation to clinical symptoms and duration of shedding: a microarray analysis of isolates from Swedish children

A Matussek  1   2 , C Jernberg  3 , I-M Einemo  4 , S Monecke  5   6   7 , R Ehricht  6   7 , I Engelmann  6   7 , S Löfgren  8 , S Mernelius  8
Affiliations

Genetic makeup of Shiga toxin-producing Escherichia coli in relation to clinical symptoms and duration of shedding: a microarray analysis of isolates from Swedish children

A Matussek et al. Eur J Clin Microbiol Infect Dis. 2017 Aug.

Abstract

Shiga toxin (Stx)-producing Escherichia coli (STECs) cause non-bloody diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome, and are the primary cause of acute renal failure in children worldwide. This study investigated the correlation of genetic makeup of STEC strains as revealed by DNA microarray to clinical symptoms and the duration of STEC shedding. All STEC isolated (n = 96) from patients <10 years of age in Jönköping County, Sweden from 2003 to 2015 were included. Isolates were characterized by DNA microarray, including almost 280 genes. Clinical data were collected through a questionnaire and by reviewing medical records. Of the 96 virulence genes (including stx) in the microarray, 62 genes were present in at least one isolate. Statistically significant differences in prevalence were observed for 21 genes when comparing patients with bloody diarrhea (BD) and with non-bloody stool (18 of 21 associated with BD). Most genes encode toxins (e.g., stx2 alleles, astA, toxB), adhesion factors (i.e. espB_O157, tir, eae), or secretion factors (e.g., espA, espF, espJ, etpD, nleA, nleB, nleC, tccP). Seven genes were associated with prolonged stx shedding; the presence of three genes (lpfA, senB, and stx1) and the absence of four genes (espB_O157, espF, astA, and intI1). We found STEC genes that might predict severe disease outcome already at diagnosis. This can be used to develop diagnostic tools for risk assessment of disease outcome. Furthermore, genes associated with the duration of stx shedding were detected, enabling a possible better prediction of length of STEC carriage after infection.

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Conflict of interest statement

Funding

This study was funded by Futurum, the Academy of Healthcare, County Council of Jönköping (FUTURUM-425271).

Conflict of interest

Stefan Monecke, Ralf Ehricht and Ines Engelmann are employees at Alere Technologies/InfectoGnostics, the company who performed the DNA-microarray analysis.

Ethical approval

Formal consent is not required, as sample and data collection is part of the routine microbiological and contact tracing work. This article does not contain any studies with animals performed by any of the authors.

Figures

Fig. 1
Fig. 1
Distribution of serotypes among STEC causing BD and NBS, ONT O-serotype non-typeable
Fig. 2
Fig. 2
MST based on microarray results of 62 virulence genes for all STEC isolates. eae is present in all strains in groups A and B but in none of the strains in group C. In group A, all strains have an stx2 subtype, and in group B 33% do. In group C, stx1 dominates and 30% harbors stx2b. All strains with serotype O157:H7 are found in group A, and O26:H11 are found in group B. Light grey represents patients with BD and dark grey patients with NBS. The length of the branches is proportional to the distance between the types. The size of the nodes represents the number of isolates included in that type
Fig. 3
Fig. 3
MST based on the microarray results of 62 virulence genes for all STEC isolates. Dark blue represents patients with a total clinical symptom score of 0, light blue = 1, purple = 2, yellow = 3, orange = 4 and red = 5. The length of the branches is proportional to the distance between the types. The size of the nodes represents the number of isolates included in that type
See this image and copyright information in PMC

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