NR AXOD
AU Head,M.; Peden,A.; Ritchie,D.; Bishop,M.; Ironside,J.
TI Pathological Investigation of Blood Donors and Recipients Linked by Transfusion-Associated Variant CJD Agent Transmission
QU International Conference - Prion 2007 (26.-28.9.2007) Edinburgh International Conference Centre, Edinburgh, Scotland, UK - Book of Abstracts: Pathology and Pathogenesis P03.129
IA http://www.prion2007.com/pdf/Prion Book of Abstracts.pdf
PT Konferenz-Poster
AB
Background: The transfusion medicine epidemiological review has recently identified blood donors who went on to develop variant CJD, and recipients of those blood donations, who subsequently developed clinical variant CJD or signs of variant CJD infection. Consequently, it now seems highly probable that variant CJD can be transmitted by blood transfusion from pre-clinical blood donors.
Objective: Secondary transmission of variant CJD has the potential to change the pathological features of the disease. Hence, we have examined the histopathology and biochemistry of the donors and recipients in the first two reported cases of blood transfusion-associated variant CJD agent transmission.
Methods: The pathological features in fixed brain and spleen specimens were examined by conventional histology and immunohistochemistry for abnormal prion protein. The form of abnormal prion protein present in frozen brain and spleen specimens were analysed by Western blotting.
Results: The pathological features found in the brain in the first reported case of transfusion-associated variant CJD transmission were qualitatively and quantitatively similar to those of the linked blood donor and of the variant CJD patient group as a whole. The prion protein Western blot analysis of brain tissue from the blood recipient was also typical of variant CJD. Biochemical and immunohistological analysis of spleen tissue from the blood donor and recipient in the second case of transfusionassociated agent transmission also closely resembled each other.
Conclusions: These limited data suggest that secondary transmission of the BSE agent in humans does not substantially alter the characteristic histopathology and biochemistry of variant CJD, at least in the most obvious aspects of brain and spleen pathology shown here. Consequently, cases of transfusion-associated secondary transmission are likely to be correctly identified as variant CJD but their aetiology may rest on epidemiological evidence.
AD M. Head, A. Peden, D. Ritchie, M. Bishop, J. Ironside, University of Edinburgh, National CJD Surveillance Unit, UK
SP englisch
PO Schottland