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From: TSS ()
Subject: Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC
Date: September 29, 2007 at 12:45 pm PST

P03.137


Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC


Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan

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.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


TSS



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