NR AXZE
AU Yamakawa,Y.; Ono,F.; Tase,N.; Terao,K.; Tannno,J.; Wada,N.; Tobiume,M.; Sato,Y.; Okemoto-Nakamura,Y.; Hagiwara,K.; Sata,T.
TI Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC
QU International Conference - Prion 2007 (26.-28.9.2007) Edinburgh International Conference Centre, Edinburgh, Scotland, UK - Book of Abstracts: Pathology and Pathogenesis P03.137
IA http://www.prion2007.com/pdf/Prion Book of Abstracts.pdf
PT Konferenz-Poster
AB Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPsc. Severe spongiform change in the brain together with heavy accumulation of PrPsc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPsc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPsc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPsc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPsc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPsc was accumulated at not only CNS but also widely distributed lymphatic tissues.
AD Y. Yamakawa, Y. Okemoto-Nakamura, K. Hagiwara, National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; F. Ono, Corporation for Production and Research Laboratory Primates., Japan; N. Tase, K. Terao, J. Tannno, National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; N. Wada, Yamauchi Univ., Veterinary Medicine, Japan; M. Tobiume, Y. Sato, T. Sata, National Institure of Infectious diseases, Pathology, Japan
SP englisch
PO Schottland
EA pdf-Datei und Poster (Posterautoren: F. Ono, K. Terao, N. Tase, A. Hiyaoka, A. Ohyama, Y. Tezuka, N. Wada, Y. Sato, M. Tobiume, Y. Nakamura-Okemoto, K. Hagiwara, Y. Yamakawa, T. Sata)