Microbiology of thrombotic microangiopathies in Scotland, 20032006
Abstract number: 1732_177
Pollock K., Locking M., Cowden J.
Without current surveillance of thrombotic microangiopathies such as HUS, neither prevalence nor outcomes are established in either adults or children. This study seeks to identify both health outcomes and existing management strategies. It comprises clinically driven enhanced surveillance of HUS and TTP and also further investigates the links between these syndromes and factors, which have been implicated in the etiology of HUS and TTP including infections, vascular procedures, chemotherapeutic agents and immuno-suppressants.
Cases were ascertained prospectively by active, national surveillance during 2003 to 2006. Consultants in haematology, infectious diseases, microbiology, nephrology, paediatrics and public health medicine, were sent a monthly e-mail with case definition and asked to indicate whether they had a `case to report' or `nil return'. Questionnaires, information sheets and consent forms were then sent to the relevant clinicians/consultants by post. All completed forms and questionnaires were returned to HPS and entered into a database for statistical analyses. From 2003 to October 2006, 145 reports of thrombotic microangiopathy were notified to HPS of which 103 were clinically designated HUS and 42 as TTP. There were 10 fatalities, 22 cases had some form of renal impairment and of those, 14 became dialysis dependent. Of 103 reports of HUS, 85 (83%) were caused by verotoxin-producing E. coli (VTEC) (82 were due to serotype O157). The non-O157 organisms were designated as serotypes O145, O177 and O-unidentifiable. Two atypical HUS cases were reported. One was preceded by parvovirus B19 infection/MMR immunisation and the other was due to infection with Streptococcus pneumoniae. The list of predisposing infections for development of TTP was more varied and included infection with coagulase-negative Staphylococcus aureus, Klebsiella pneumoniae and Clostridium difficile but development of TTP was significantly associated with severe sepsis. The study clearly demonstrates that development of HUS or TTP has serious and sometimes fatal consequences and that infection is a major predisposing factor in development of such syndromes.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
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