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Different prion disease phenotypes result from inoculation of cattle with two temporally separated sources of sheep scrapie from Great Britain.

Konold T, Lee YH, Stack MJ, Horrocks C, Green RB, Chaplin M, Simmons MM, Hawkins SA, Lockey R, Spiropoulos J, Wilesmith JW, Wells GA - BMC Vet. Res. (2006)

Bottom Line: Disease occurred in 16 cattle, nine inoculated with the pre-1975 inoculum and seven inoculated with the post-1990 inoculum, with four cattle still alive at 83 months post challenge (as at June 2006).The different inocula produced predominantly two different disease phenotypes as determined by histopathological, immunohistochemical and Western immunoblotting methods and biological characterisation on transmission to mice, neither of which was identical to BSE.The study has demonstrated that cattle inoculated with different pooled scrapie sources can develop different prion disease phenotypes, which were not consistent with the phenotype of BSE of cattle and whose isolates did not have the strain typing characteristics of the BSE agent on transmission to mice.

View Article: PubMed Central - HTML - PubMed

Affiliation: Veterinary Laboratories Agency Weybridge, New Haw, Addlestone, UK. t.konold@vla.defra.gsi.gov.uk

ABSTRACT

Background: Given the theoretical proposal that bovine spongiform encephalopathy (BSE) could have originated from sheep scrapie, this study investigated the pathogenicity for cattle, by intracerebral (i.c.) inoculation, of two pools of scrapie agents sourced in Great Britain before and during the BSE epidemic. Two groups of ten cattle were each inoculated with pools of brain material from sheep scrapie cases collected prior to 1975 and after 1990. Control groups comprised five cattle inoculated with sheep brain free from scrapie, five cattle inoculated with saline, and for comparison with BSE, naturally infected cattle and cattle i.c. inoculated with BSE brainstem homogenate from a parallel study. Phenotypic characterisation of the disease forms transmitted to cattle was conducted by morphological, immunohistochemical, biochemical and biological methods.

Results: Disease occurred in 16 cattle, nine inoculated with the pre-1975 inoculum and seven inoculated with the post-1990 inoculum, with four cattle still alive at 83 months post challenge (as at June 2006). The different inocula produced predominantly two different disease phenotypes as determined by histopathological, immunohistochemical and Western immunoblotting methods and biological characterisation on transmission to mice, neither of which was identical to BSE. Whilst the disease presentation was uniform in all scrapie-affected cattle of the pre-1975 group, the post-1990 inoculum produced a more variable disease, with two animals sharing immunohistochemical and molecular profile characteristics with animals in the pre-1975 group.

Conclusion: The study has demonstrated that cattle inoculated with different pooled scrapie sources can develop different prion disease phenotypes, which were not consistent with the phenotype of BSE of cattle and whose isolates did not have the strain typing characteristics of the BSE agent on transmission to mice.

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Average lesion profiles in RIII mice for each inoculum and comparison with BSE. G1 Dorsal medulla nuclei. G2 Cerebellar cortex. G3 Superior colliculus. G4 Hypothalamus. G5 Central thalamus. G6 Hippocampus. G7 Lateral septal nuclei. G8 Cerebral cortex (at the level of the thalamus). G9 Cerebral cortex (at the level of the septal nuclei). W1 Cerebellar white matter. W2 Tegmentum. W3 Pyramidal tract.
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Figure 11: Average lesion profiles in RIII mice for each inoculum and comparison with BSE. G1 Dorsal medulla nuclei. G2 Cerebellar cortex. G3 Superior colliculus. G4 Hypothalamus. G5 Central thalamus. G6 Hippocampus. G7 Lateral septal nuclei. G8 Cerebral cortex (at the level of the thalamus). G9 Cerebral cortex (at the level of the septal nuclei). W1 Cerebellar white matter. W2 Tegmentum. W3 Pyramidal tract.

Mentions: The lesion profiles in RIII mice and their comparison with BSE are given in Figure 11. Similarities with respect to the shape of the profiles are seen between the three cattle of the pre-1975 group (peaks at grey matter areas 3, 5 and 7), between the two cattle of the post-1990 group (peaks at grey matter areas 5 and 7) and between the original pre-1975 inoculum and the average BSE in mice (peaks at grey matter areas 1, 4 and 7), although for BSE the average lesion scores in the hypothalamus and lateral septal nuclei were considerably lower (approximately half) compared to the pre-1975 inoculum. Cluster analysis clearly separated individual cattle of the pre-1975 or post-1990 group from the original pre-1975 inoculum and natural BSE. The differences, expressed as Euclidian distances, were much smaller between the different BSE pools than between BSE and the pre-1975 inoculum (Figure 2B).


Different prion disease phenotypes result from inoculation of cattle with two temporally separated sources of sheep scrapie from Great Britain.

Konold T, Lee YH, Stack MJ, Horrocks C, Green RB, Chaplin M, Simmons MM, Hawkins SA, Lockey R, Spiropoulos J, Wilesmith JW, Wells GA - BMC Vet. Res. (2006)

Average lesion profiles in RIII mice for each inoculum and comparison with BSE. G1 Dorsal medulla nuclei. G2 Cerebellar cortex. G3 Superior colliculus. G4 Hypothalamus. G5 Central thalamus. G6 Hippocampus. G7 Lateral septal nuclei. G8 Cerebral cortex (at the level of the thalamus). G9 Cerebral cortex (at the level of the septal nuclei). W1 Cerebellar white matter. W2 Tegmentum. W3 Pyramidal tract.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC1636635&req=5

Figure 11: Average lesion profiles in RIII mice for each inoculum and comparison with BSE. G1 Dorsal medulla nuclei. G2 Cerebellar cortex. G3 Superior colliculus. G4 Hypothalamus. G5 Central thalamus. G6 Hippocampus. G7 Lateral septal nuclei. G8 Cerebral cortex (at the level of the thalamus). G9 Cerebral cortex (at the level of the septal nuclei). W1 Cerebellar white matter. W2 Tegmentum. W3 Pyramidal tract.
Mentions: The lesion profiles in RIII mice and their comparison with BSE are given in Figure 11. Similarities with respect to the shape of the profiles are seen between the three cattle of the pre-1975 group (peaks at grey matter areas 3, 5 and 7), between the two cattle of the post-1990 group (peaks at grey matter areas 5 and 7) and between the original pre-1975 inoculum and the average BSE in mice (peaks at grey matter areas 1, 4 and 7), although for BSE the average lesion scores in the hypothalamus and lateral septal nuclei were considerably lower (approximately half) compared to the pre-1975 inoculum. Cluster analysis clearly separated individual cattle of the pre-1975 or post-1990 group from the original pre-1975 inoculum and natural BSE. The differences, expressed as Euclidian distances, were much smaller between the different BSE pools than between BSE and the pre-1975 inoculum (Figure 2B).

Bottom Line: Disease occurred in 16 cattle, nine inoculated with the pre-1975 inoculum and seven inoculated with the post-1990 inoculum, with four cattle still alive at 83 months post challenge (as at June 2006).The different inocula produced predominantly two different disease phenotypes as determined by histopathological, immunohistochemical and Western immunoblotting methods and biological characterisation on transmission to mice, neither of which was identical to BSE.The study has demonstrated that cattle inoculated with different pooled scrapie sources can develop different prion disease phenotypes, which were not consistent with the phenotype of BSE of cattle and whose isolates did not have the strain typing characteristics of the BSE agent on transmission to mice.

View Article: PubMed Central - HTML - PubMed

Affiliation: Veterinary Laboratories Agency Weybridge, New Haw, Addlestone, UK. t.konold@vla.defra.gsi.gov.uk

ABSTRACT

Background: Given the theoretical proposal that bovine spongiform encephalopathy (BSE) could have originated from sheep scrapie, this study investigated the pathogenicity for cattle, by intracerebral (i.c.) inoculation, of two pools of scrapie agents sourced in Great Britain before and during the BSE epidemic. Two groups of ten cattle were each inoculated with pools of brain material from sheep scrapie cases collected prior to 1975 and after 1990. Control groups comprised five cattle inoculated with sheep brain free from scrapie, five cattle inoculated with saline, and for comparison with BSE, naturally infected cattle and cattle i.c. inoculated with BSE brainstem homogenate from a parallel study. Phenotypic characterisation of the disease forms transmitted to cattle was conducted by morphological, immunohistochemical, biochemical and biological methods.

Results: Disease occurred in 16 cattle, nine inoculated with the pre-1975 inoculum and seven inoculated with the post-1990 inoculum, with four cattle still alive at 83 months post challenge (as at June 2006). The different inocula produced predominantly two different disease phenotypes as determined by histopathological, immunohistochemical and Western immunoblotting methods and biological characterisation on transmission to mice, neither of which was identical to BSE. Whilst the disease presentation was uniform in all scrapie-affected cattle of the pre-1975 group, the post-1990 inoculum produced a more variable disease, with two animals sharing immunohistochemical and molecular profile characteristics with animals in the pre-1975 group.

Conclusion: The study has demonstrated that cattle inoculated with different pooled scrapie sources can develop different prion disease phenotypes, which were not consistent with the phenotype of BSE of cattle and whose isolates did not have the strain typing characteristics of the BSE agent on transmission to mice.

Show MeSH
Related in: MedlinePlus