NR AFZU
AU Jeffrey,M.J.; Scott,J.R.; Williams,A.; Fraser,H.
TI Ultrastructural features of spongiform encephalopathy transmitted to mice from three species of bovidae
QU Acta Neuropathologica 1992; 84(5): 559-69
PT journal article
AB The ultrastructural neuropathology of mice experimentally inoculated with brain tissue of nyala (Tragelaphus angasi; subfamily Bovinae), or kudu (Tragelaphus strepsiceros; subfamily Bovinae) affected with spongiform encephalopathy was compared with that of mice inoculated with brain tissue from cows (Bos taurus; subfamily Bovinae) with bovine spongiform encephalopathy (BSE). As fresh brain tissue was not available for nyala or kudu, formalin-fixed tissues were used for transmission from these species. The effect of formalin fixation was compared with that of fresh brain in mice inoculated with fixed and unfixed brain tissue from cows with BSE. The nature and distribution of the pathological changes were similar irrespective of the source of inoculum or whether the inoculum was from fresh or previously fixed tissue. Vacuolation caused by loss of organelles and swelling was present in dendrites and axon terminals. Vacuoles were also seen as double-membrane-bound and single-membrane-bound structures within myelinated fibres, axon terminals and dendrites. Vacuoles are considered to have more than one morphogenesis but the structure of vacuoles in this study was nevertheless similar to previous descriptions of spongiform change in naturally occurring and experimental scrapie, Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome and kuru. Other features of the ultrastructural pathology of the transmissible spongiform encephalopathies including dystrophic neurites and scrapie-associated particles or tubulovesicular bodies were also found in this study. Neuronal autophagy was a conspicuous finding. It is suggested that excess prion protein (PrP) accumulation, or accumulation of the scrapie-associated protease-resistant isoform of PrP, may lead to localised sequestration and phagocytosis of neuronal cytoplasm and ultimately to neuronal loss.
IN Die Autoren verglichen neuropathologisch die Schädigungsmuster von Mäusen, die nach Inokulation von Hirnhomogenaten erkrankt waren, welche von BSE-kranken Rindern sowie von zwei den ebenfalls an spongiformen Encephalopathien erkrankten Antilopen stammten. Dabei handelte es sich um einen am 18.6.1986 in einem britischen Zoo gestorbenen Nyala-Buschbock (Tragelaphus angasi) [ASYI,AGMP] und die großen Kudu-Waldantilope (Tragelaphus strepsiceros) Linda (11.2.87-18.8.89) [AGMT,APBH,AGMS,AGMP]. Die Schädigungsprofile ähnelten sich und sprachen insofern für BSE-Infektionen bei beiden Antilopen.
MH Animal; Axons/ultrastructure; Brain/pathology; Cattle; Comparative Study; Dendrites/ultrastructure; Formaldehyde; Histocytochemistry; Mice; Mice, Inbred Strains; Microscopy, Electron; Prion Diseases/*pathology; Ruminants/*physiology
AD Martin J. Jeffrey (m.jeffrey@vla.maff.gov.uk), VLA Lasswade Veterinary Laboratory, Pentlands Science Park, Bush Loan, Penicuik, Edinburgh EH26 OPZ, Scotland, UK; J. R. Scott, Hugh Fraser (HughFraser@bbsrc.ac.uk), Institute for Animal Health, BBSRC and MRC, Neuropathogenesis Unit, Ogston Building, West Mains Road, Edinburgh EH9 3JF, Scotland, UK
SP englisch
PO Deutschland