NR AWGI
AU Hagiwara,K.; Nakamura,Y.; Yamakawa,Y.; Sato,Y.; Tobiume,M.; Sata,T.; et al.
AK Expert Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare (MHLW)
TI Studies on the second atypical BSE case in a Japanese black cow
QU International Conference - Prion 2006: Strategies, advances and trends towards protection of society - 3.10.-6.10.2006, Torino, Italy, Lingotto Conference Centre - Poster sessions PR-18
PT Konferenz-Poster
AB
An ELISA (Plateria, BioRad) positive specimen of a 14 year-old Japanese Black cow (beef cattle) slaughtered in an abattoir was examined by western-blot (WB) and histological/immunohistochemical (IHC) analyses for the confirmation of BSE. Dysstasia had been reported as a clinical symptom. Histological examination of the medulla oblongata at the level of obex showed severe vacuolations in dorsal nucleus of the vagus, nucleus of the solitary tract and nucleus of the spinal tract. Granular and linear deposition of PrPsc was also detected in these areas by IHC analysis. Thus, histological and IHC data were compatible with the histopathology of the typical BSE. In the WB analysis, however, the amount of the di-glycosylated PK-resistant PrPsc was found to be at approx.35% of the total PrPsc, and the mono-glycosylated PrPsc was at approx.40%. The WB analyses showed that PrPsc distributed widely in the brain with the unchanged glycosylation ratio. Such a glycosylation-ratio is distinct from that of the typical BSE agent in which the di-glycosylated form is dominant (approx.70%) but, intriguingly, similar to that of the type-2 sporadic CJD agent. No DNA mutation was detected in the PrP coding region, except polymorphisms of the codons for Gln78 and Asn192 being determined as CAG and AAT, respectively. Judging from the glycosylation-ratio, BSE prion herein is different from the typical BSE prion, and the atypical BSE prion found previously in a Holstein steer in Japan (ref. 1). Instead, its molecular feature is close, if not identical, to PrPsc found in the cattle succumbed to bovine amyloidtic spongiform encephalopathy (ref. 2), and to the sporadic CJD-like PrPsc in the mice inoculated with BSE agent (ref. 3).
References: 1) Y. Yamakawa et.al., Jpn.J.Infect.Dis. (2003), 56, 221. 2) C. Casalone et.al., PNAS (2004), 101, 3065. 3) S.E. Lloyd et.al., J.Gen.Virol. (2004), 85, 2471.
AD K. Hagiwara, Y. Nakamura, Y. Yamakawa: Dep. Biochemistry and Cell Biology, Natl. Inst. Infectious Diseases, Shinjuku, Tokyo 162-8640, Japan; Y. Sato, M. Tobiume, T. Sata: Dep. Pathology, Natl. Inst. Infectious Diseases, Shinjuku, Tokyo 162-8640, Japan; Expert Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare (MHLW): Tokyo 100-8916, Japan 3. E-mail: hagiwark@nih.go.jp
SP englisch
PO Italien