Open Access Highly Accessed Original research

Clinical aspects of a nationwide epidemic of severe haemolytic uremic syndrome (HUS) in children

Lars Krogvold1*, Thore Henrichsen1, Anna Bjerre2, Damien Brackman3, Henrik Dollner4, Helga Gudmundsdottir5, Gaute Syversen6, Pål Aksel Næss7 and Hans Jacob Bangstad1

Author Affiliations

1 Department of Paediatrics, Oslo University hospital, Ulleval, Kirkeveien 166, 0407 Oslo, Norway

2 Department of Paediatrics, Section for Specialised Medicine, Oslo University Hospital, Rikshospitalet, Norway

3 Department of Paediatrics, Haukeland Hospital, Bergen, Norway

4 Children's Department, St. Olavs University Hospital of Trondheim, Institute of Laboratory Medicine, Children's and Women's Health, Norwegian University of Science and Technology, Trondheim, Norway

5 Nephrological Department, Oslo University Hospital, Ulleval, Norway

6 Department of Microbiology, Oslo University Hospital, Ulleval, Norway

7 Department of Paediatric Surgery, Oslo University Hospital, Ulleval, Norway

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Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2011, 19:44  doi:10.1186/1757-7241-19-44

Published: 28 July 2011

Abstract

Background

Report a nationwide epidemic of Shiga toxin-producing E. coli (STEC) O103:H25 causing hemolytic uremic syndrome (D+HUS) in children.

Methods

Description of clinical presentation, complications and outcome in a nationwide outbreak.

Results

Ten children (median age 4.3 years) developed HUS during the outbreak. One of these was presumed to be a part of the outbreak without microbiological proof. Eight of the patients were oligoanuric and in need of dialysis. Median need for dialysis was 15 days; one girl did not regain renal function and received a kidney transplant. Four patients had seizures and/or reduced consciousness. Cerebral oedema and herniation caused the death of a 4-year-old boy. Two patients developed necrosis of colon with perforation and one of them developed non-autoimmune diabetes.

Conclusion

This outbreak of STEC was characterized by a high incidence of HUS among the infected children, and many developed severe renal disease and extrarenal complications. A likely explanation is that the O103:H25 (eae and stx2-positive) strain was highly pathogen, and we suggest that this serotype should be looked for in patients with HUS caused by STEC, especially in severe forms or outbreaks.