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Nationwide study of haemolytic uraemic syndrome: clinical, microbiological, and epidemiological features
  1. E J Elliotta,
  2. R M Robins-Browned,
  3. E V O'Loughlinb,
  4. V Bennett-Woodd,
  5. J Bourkef,
  6. P Henningg,
  7. G G Hoggh,
  8. J Knightc,
  9. H Powelle,
  10. D Redmondi,
  11. Contributors to the Australian Paediatric Surveillance Unit
  1. aDepartment of Paediatrics and Child Health, University of Sydney and The Children's Hospital at Westmead, Sydney, Australia, bDepartment of Gastroenterology, The Children's Hospital at Westmead, cCentre for Kidney Research, The Children's Hospital at Westmead, dMicrobiological Research Unit, Department of Microbiology and Infectious Diseases, Royal Children's Hospital, Melbourne, eDepartment of Nephrology, Royal Children's Hospital, Melbourne, fRoyal Children's Hospital, Mater Hospital and Princess Alexandra Hospital, Brisbane, Queensland, Australia, gWomen's and Children's Hospital, Adelaide, hMicrobiological Diagnostic Unit, Department of Microbiology and Immunology, University of Melbourne, iAustralian Paediatric Surveillance Unit
  1. A/Prof E Elliott, Dept of Paediatrics and Child Health University of Sydney, c/o The Children's Hospital at Westmead, Locked Bag 4001, Westmead, NSW, 2145, Australiaelizabe2{at}chw.edu.au

Abstract

AIMS To establish the incidence and aetiology of haemolytic uraemic syndrome (HUS) in Australia and compare clinical and microbial characteristics of sporadic and outbreak cases.

METHODS National active surveillance through the Australian Paediatric Surveillance Unit with monthly case notification from paediatricians, July 1994 to June 1998. Children under 15 years presenting with microangiopathic haemolytic anaemia, thrombocytopenia, and acute renal impairment were identified.

RESULTS Ninety eight cases were identified (incidence 0.64 per 105 children <15 years/annum and 1.35 per 105 children <5 years/annum). Eighty four were associated with diarrhoea (64 sporadic, 20 constituting an outbreak) and 14 were atypical. Shiga toxin producingEscherichia coli (STEC) O111:H− was the most common isolate in sporadic HUS and caused the outbreak. However O111:H− isolates from outbreak and sporadic cases differed in phage type and subtyping by DNA electrophoresis. STEC isolates from sporadic cases included O26:H−, O113:H21, O130:H11, OR:H9, O157:H−, ONT:H7, and ONT:H−. STEC O157:H7 was not isolated from any case. Only O111:H− isolates produced both Shiga toxins 1 and 2 and possessed genes encoding E coli attaching and effacing gene (intimin) and enterohemolysin. Outbreak cases had worse gastrointestinal and renal disease at presentation and more extrarenal complications.

CONCLUSIONS Linking national surveillance with a specialised laboratory service allowed estimation of HUS incidence and provided information on its aetiology. In contrast to North America, Japan, and the British Isles, STEC O157:H7 is rare in Australia; however, non-O157:H7 STEC cause severe disease including outbreaks. Disease severity in outbreak cases may relate to yet unidentified virulence factors of the O111:H− strain isolated.

  • Shiga toxin
  • E coli
  • haemolytic uraemic sydrome
  • surveillance

https://doi.org/10.1136/adc.85.2.125

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