NR ATPO

AU Füzi,M.

TI Are scrapie and chronic wasting disease transmitted by an intermediate host under natural conditions?

QU International Conference - Prion 2005: Between fundamentals and society's needs - 19.10.-21.10.2005, Congress Center Düsseldorf - Poster Session: Pathogenesis PATH-25

PT Konferenz-Poster

AB It is well established that scrapie of sheep and goat and chronic wasting disease /CWD/ of cervids, unlike other forms of prion disease /bovine spongiform encephalopathy, feline spongiform encephalopathy, spongiform encephalopathy of minks, Creutzfeldt-Jakob disease/, transmit by contact under natural conditions. Studies on the pathogenesis of both scrapie and CWD indicate that natural infection occurs via the alimentary tract. Moreover, recent epidemiological observations with CWD strongly suggest that the agent is shed from the alimentary tract and shedding is progressive in the course of disease. However, no report convincingly demonstrating infectivity in either the faeces or the saliva of cervids with CWD and of sheep and goat with scrapie has been published. What can account for the diverse epidemiology of prion disease in various species and the apparent lack of infectivity in the faeces of cervids with CWD and sheep and goat with scrapie? The most probable explanation is that an intermediate host, a vector, is responsible for the transmission of prion disease to sheep, goat and cervids under natural conditions. This intermediate host must have a restricted host range and may, thus, be incapable of transmitting prion disease to other species like cattle, cat, mink or hunman. The existence of this hypothetical intermediate host is also supported by earlier epidemiological observations which suggest that while scrapie acquired under natural conditions transmits horizontally, artificially-induced disease is not contagious in sheep and goat. In addition, it is well-known that maternal transmission of scrapie /which is certainly a perinatal form of contact infection/ occurs exclusively in animals with the natural form of the disease. The identification of the hypothetical intermediate host could substantially further our understanding of the pathogenesis of prion disease.

AD M.Füzi, National Center for Epidemiology, Budapest, Hungary

SP englisch

PO Deutschland

EA Bild 1, Bild 2, Bild 3

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