NDT Plus Advance Access originally published online on April 14, 2008
NDT Plus 2008 1(4):274-275; doi:10.1093/ndtplus/sfn032
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A case of lethal enteroviral haemolytic uraemic syndrome?
Institute of Forensic Medicine, University of Aarhus, Denmark
Correspondence: E-mail: Shoaibafzal{at}hotmail.com
Sir,
In the recent years much has been learnt about haemolytic uraemic syndrome (HUS), which is defined by symptomatic or bloody diarrhoea, acute nephropathy, thrombocytopenia and microangiopathic haemolytic anaemia. Often HUS is complicated by neurological symptoms in children [1]. The main aetiological culprit is Shiga-like toxin-producing E. coli (STEC) accounting for 
85% of HUS cases. Recently the aetiological role of enteroviruses in HUS has been studied and rejected as being an aetiological agent [3] even though earlier case reports suggested a role (see references in [3]). We present a case of HUS, which was probably due to enteroviral infection.
A 17-month-old girl, who was previously healthy, was admitted with bloody diarrhoea preceded by vomiting for a day or two. A few hours into the admission the girl developed a seizure and was transferred to an ICU. Extensive clinical and laboratory testing was carried out (Table 1). Tests showed uraemia, thrombocytopenia, haemolytic anaemia, leucocytosis and anuria. The patient developed cardiac arrest at 8 h into the admission. Resuscitation with concurrent peritoneal dialysis was attempted for an hour without success.
On autopsy we found a normally developed girl without any deformities. The autopsy revealed a thickened haemorrhagic colon, stasis and oedema in the lungs, hydrothorax and hydroperitoneum. The CNS was without lesions (vascular or any other). There were no signs of iatrogenic injury.
On histopathological examination we found signs of endothelial damage in the small vessels of the kidneys (Figure 1) and the intestine (with thrombosis), fragments of thrombi in the small lung vessels and a necrotic colon with submucosal haemorrhage and leukocyte infiltration. No thrombi were found in the brain.
Concurrent to the autopsy we requested several tests expecting to find a STEC infection but instead we found an enteroviral infection (Table 1).
Our case indicates that enteroviral infections may be able to inflict HUS, and contradicts other studies of HUS [3].
It is clear from the above-mentioned findings that the case presented as HUS, with all of its cardinal findings, uraemia, thrombocytopenia, haemolytic anaemia, and endothelial damage in the kidney and intestine. We used stool and tissue cultures for the bacterial tests whereas viral tests included PCR, serology and cultures. Sadly subtyping (using cell cultures) was unsuccessful after several attempts.
A weakness in our report is that we do not have multiple tests (i.e. serology) to exclude a STEC infection, only a standard stool culture. Furthermore, one could speculate that the finding of enteroviral RNA is coincidental or from "leakage" of colonic virus into blood.
In support of our conclusion, enteroviruses are known to be able to infect colonic cells and endothelial cells, and damage both by either lytic or immunological mechanisms, the prerequisites for inducing HUS [4,5]. Furthermore our detection techniques are more sensitive [6,7] than the ones used earlier in studies [3].
Our case underlines the need for a large-scale epidemiological investigation of STEC-negative HUS cases using the most recent sensitive diagnostic tests especially considering the poorer prognosis of STEC-negative cases [3].
Conflict of interest statement. None declared.
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