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Location: BACLIFF, Texas, United States

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

Monday, December 24, 2007

Pathogenesis of bovine spongiform encephalopathy in sheep

Pathogenesis of bovine spongiform encephalopathy in sheep

L. J. M. van Keulen1 , M. E. W. Vromans1, C. H. Dolstra1, A. Bossers1 and F. G. van Zijderveld1

(1) Department of Bacteriology and TSE’s, Central Institute for Animal Disease Control (CIDC), Wageningen University and Research Centre, P.O. Box 2004, 8203 AA Lelystad, The Netherlands

Received: 16 August 2007 Accepted: 27 November 2007 Published online: 19 December 2007

Abstract The pathogenesis of bovine spongiform encephalopathy (BSE) in sheep was studied by immunohistochemical detection of scrapie-associated prion protein (PrPSc) in the gastrointestinal, lymphoid and neural tissues following oral inoculation with BSE brain homogenate. First accumulation of PrPSc was detected after 6 months in the tonsil and the ileal Peyer’s patches. At 9 months postinfection, PrPSc accumulation involved all gut-associated lymphoid tissues and lymph nodes as well as the spleen. At this time point, PrPSc accumulation in the peripheral neural tissues was first seen in the enteric nervous system of the caudal jejunum and ileum and in the coeliac-mesenteric ganglion. In the central nervous system, PrPSc was first detected in the dorsal motor nucleus of the nervus Vagus in the medulla oblongata and in the intermediolateral column in the spinal cord segments T7–L1. At subsequent time points, PrPSc was seen to spread within the lymphoid system to also involve all non-gut-associated lymphoid tissues. In the enteric nervous system, further spread of PrPSc involved the neural plexi along the entire gastrointestinal tract and in the CNS the complete neuraxis. These findings indicate a spread of the BSE agent in sheep from the enteric nervous system through parasympathetic and sympathetic nerves to the medulla oblongata and the spinal cord.

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L. J. M. van Keulen Email:



In this study, we investigated the pathogenesis of a BSE infection in sheep by following the accumulation of PrPSc in sheep killed at various time points during the incubation period of BSE. The first tissues to accumulate PrPSc were the lymphoid tissues of the GALT, followed by the GALT-draining lymph nodes and the spleen and, at a later stage, the non-GALT lymph nodes. The temporal spread and pattern of PrPSc deposition in the lymphoid tissues were similar to those described previously for natural scrapie [21, 22]. In the spleen of the BSE-infected sheep, however, a more abundant accumulation of PrPSc was seen in macrophages of the marginal zone. This probably reflects an active trapping and phagocytosis of PrPSc during a systemic circulation of the BSE agent. This is in agreement with the studies of Houston et al., who demonstrated the presence of infectivity in the blood of orally BSE-infected sheep, both in the preclinical and clinical phase, by the transmission of BSE to TSE-free recipients through whole-blood transfusion [12, 14]. The question remains which fraction of the blood contains BSE infectivity and thus whether the BSE agent is present in blood plasma or whether it is associated with a cellular component of the blood. Preliminary results from transfusion with blood fractions have shown infectivity in the buffy coat but could not exclude infectivity in plasma and/or red cell fractions [14].

The first peripheral nervous tissues to accumulate PrPSc in the pathogenesis of BSE in sheep were the post-ganglionic parasympathetic motor neurons in the submucosal and myenteric plexi of the ENS and the post-ganglionic sympathetic motor neurons in the coeliac-mesenteric ganglion. The first accumulations of PrPSc in the CNS were detected in the pre-ganglionic parasympathetic motor neurons of the DMNV in the brain stem and in the pre-ganglionic sympathetic motor neurons of the IMLC in the spinal cord. From these initial sites of PrPSc accumulation in the peripheral and central nervous system, PrPSc subsequently spread to involve the entire ENS and CNS. This pathogenetic route of the BSE agent from the ENS through the efferent motor fibers of the autonomic nervous system to the CNS is similar to the pathogenesis of natural scrapie in sheep [20]. In scrapie- and BSE-infected sheep, the preceding infection of the Peyer’s patches could possibly play a role in facilitating the infection of the post-ganglionic motor neurons of the ENS. In cattle orally exposed to BSE, infectivity has also been found in the Peyer’s patches of the ileum [23, 24]. Preliminary observations on the pathogenesis of BSE in cattle indicate a similar spread of the BSE agent from the gut through the efferent autonomic nervous system to the CNS [11]. However, the role of the ENS in the pathogenesis of BSE in cattle is still obscure as PrPSc was not found in the ENS during the early stages of a BSE infection and only sparsely in the myenteric plexus of cattle in the end stage of BSE [18].

The results of the present study can be compared with previous time course studies on BSE in sheep in which the same dose and the same BSE brain homogenate were used for oral inoculation of ARQ/ARQ Romney sheep. In these studies, infectivity was detected by bio-assay in RIII mice in the Peyer’s patches at 4 mpi [2]. In contrast, at this time point, PrPSc was detected immunohistochemically only in the retropharyngeal lymph node and not in the Peyer’s patches [2, 15]. In our study of ARQ/ARQ Texel sheep, we detected sparse deposits of PrPSc at 6 mpi in both the tonsil and Peyer’s patches that were only detected after thorough screening of the entire tissue by examining sections every 50 µm until the blocks were exhausted. This might explain the difference with the immunohistochemical studies in the Romney sheep where PrPSc was only detected in the retropharyngeal lymph node, but it is in general agreement with the bio-assay, where infectivity was found in the Peyer’s patches at 4 mpi (but not in the tonsil). In the Texel sheep killed at 9 mpi, all GALT tissues, the spleen, ENS, IMLC and DMNV were positive for PrPSc, whereas in the Romney sheep at 10 mpi, PrPSc was only detected in the retropharyngeal lymph node, and infectivity was only detected in the spleen. This indicates a more rapid spread of the BSE infection in the Texel sheep compared to the Romney sheep, since both the dose and the inoculum were the same in the two studies. Because the age at inoculation and the PrP genotypes of the animals in both studies were also the same, the differences in the temporal spread of the BSE agent between the two breeds must be related to other genetic factors outside the PrP region, or to other unknown breed factors. In the Romney sheep, the BSE agent only became widespread at 16 mpi when PrPSc and infectivity were detected in a wide range of nervous tissues, lymphoreticular tissues and viscera including the liver. PrPSc in the liver was reported to be present within Kupffer cells at several stages of the BSE infection (M. Jeffrey, personal communication). In the Texel sheep however, no PrPSc was detected in Kupffer cells or hepatocytes at any stage during the BSE infection.

At present, active surveillance of TSE in sheep and goats has been increased in the EU (EU regulation 214/2005) because of the finding of a BSE-infected goat in France [7] and possibly in the UK (confirmation by strain typing is still pending) [16]. Several rapid tests for TSEs in small ruminants are now available (EU regulation 260/2005), all of which use the medulla oblongata, and in particular, the obex region as source material for testing. In the present study, we detected PrPSc in the DMNV at the obex of BSE-infected sheep from 9 mpi. In a previous study of natural scrapie in sheep, PrPSc was detected in the DMNV in sheep from 10 months of age [20]. Therefore, preclinically TSE-infected animals are likely to be identified through rapid testing as long as the DMNV region in the obex is excised and used for rapid testing. Further biochemical and/or immunohistochemical tests can then be used to differentiate BSE from scrapie infection, while final confirmation of the TSE strain will still require bio-assay in mice.

Acknowledgments We would like to thank Dr Martin Jeffrey for supplying the BSE brain homogenate. This work was supported by the EU (FAIR CT 98-7006) and the Dutch Ministry of Agriculture, Nature and Food Quality. Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.


1. Bellworthy SJ, Dexter G, Stack M, Chaplin M, Hawkins SA, Simmons MM, Jeffrey M, Martin S, Gonzalez L, Hill P (2005) Natural transmission of BSE between sheep within an experimental flock. Vet Rec 157:206

2. Bellworthy SJ, Hawkins SA, Green RB, Blamire I, Dexter G, Dexter I, Lockey R, Jeffrey M, Ryder S, Berthelin Baker C, Simmons MM (2005) Tissue distribution of bovine spongiform encephalopathy infectivity in Romney sheep up to the onset of clinical disease after oral challenge. Vet Rec 156:197–202

3. Bruce ME, Chree A, McConnell I, Foster JD, Pearson GR, Fraser H (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice:strain variation and the species barrier. Phil Trans R Soc Lond B 343:405–411

4. Bruce ME, Will RG, Ironside JWW, McConnell I, Drummond D, Suttie A, McCardle L, Chree A, Hope J, Birkett CR, Cousens SN, Fraser H, Bostock CJ (1997) Transmissions to mice indicate that ‘new variant’ CJD is caused by the BSE agent. Nature 389:498–501

5. Buschmann A, Luhken G, Schultz J, Erhardt G, Groschup MH (2004) Neuronal accumulation of abnormal prion protein in sheep carrying a scrapie-resistant genotype (PrPARR/ARR). J Gen Virol 85:2727–2733

6. Buschmann A, Groschup MH (2005) Highly bovine spongiform encephalopathy-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J Infect Dis 192:934–942

7. Eloit M, Adjou K, Coulpier M, Fontaine JJ, Hamel R, Lilin T, Messiaen S, Andreoletti O, Baron T, Bencsik A, Biacabe AG, Beringue V, Laude H, Le Dur A, Vilotte JL, Comoy E, Deslys JP, Grassi J, Simon S, Lantier F, Sarradin P (2005) BSE agent signatures in a goat. Vet Rec 156:523–524

8. Foster JD, Hope J, Fraser H (1993) Transmission of bovine spongiform encephalopathy to sheep and goats. Vet Rec 133:339–341

9. Foster JD, Bruce ME, McConnell I, Chree A, Fraser H (1996) Detection of BSE infectivity in brain and spleen of experimentally infected sheep. Vet Rec 138:546–548

10. Fraser H, Foster JD (1993) Transmission to mice sheep and goats and bioassay of bovine tissues. In: Transmissible spongiform encephalopathies. A consultation on BSE with the Scientific Veterinary Committee of the Commission of the European Communities, Brussels. Kluwer Academics, Dordrecht, pp 145–159

11. Hoffmann C, Ziegler U, Buschmann A, Weber A, Kupfer L, Oelschlegel A, Hammerschmidt B, Groschup MH (2007) Prions spread via the autonomic nervous system from the gut to the central nervous system in cattle incubating bovine spongiform encephalopathy. J Gen Virol 88:1048–1055

12. Houston F, Foster JD, Chong A, Hunter N, Bostock CJ (2000) Transmission of BSE by blood transfusion in sheep. Lancet 356:999–1000

13. Houston F, Goldmann W, Chong A, Jeffrey M, Gonzalez L, Foster J, Parnham D, Hunter N (2003) Prion diseases: BSE in sheep bred for resistance to infection. Nature 423:498

14. Hunter N, Foster J, Chong A, McCutcheon S, Parnham D, Eaton S, MacKenzie C, Houston F (2002) Transmission of prion diseases by blood transfusion. J Gen Virol 83:2897–2905

15. Jeffrey M, Ryder S, Martin S, Hawkins SA, Terry L, Berthelin-Baker C, Bellworthy SJ (2001) Oral inoculation of sheep with the agent of bovine spongiform encephalopathy (bse). 1. onset and distribution of disease-specific prp accumulation in brain and viscera. J Comp Pathol 124:280–289

16. Jeffrey M, Martin S, Gonzalez L, Foster J, Langeveld JP, van Zijderveld FG, Grassi J, Hunter N (2006) Immunohistochemical features of PrP(d) accumulation in natural and experimental goat transmissible spongiform encephalopathies. J Comp Pathol 134:171–181

17. Pearson GRR, Wyatt JM, Gruffydd Jones TJ, Hope J, Chong A, Higgins RJ, Scott AC, Wells GAH (1992) Feline spongiform encephalopathy: fibril and PrP studies. Vet Rec 131:307–310

18. Terry LA, Marsh S, Ryder SJ, Hawkins SA, Wells GA, Spencer YI (2003) Detection of disease-specific PrP in the distal ileum of cattle exposed orally to the agent of bovine spongiform encephalopathy. Vet Rec 152:387–392

19. Thuring CM, van Keulen LJ, Langeveld JP, Vromans ME, van Zijderveld FG, Sweeney T (2005) Immunohistochemical distinction between preclinical bovine spongiform encephalopathy and scrapie infection in sheep. J Comp Pathol 132:59–69

20. van Keulen LJ, Schreuder BE, Vromans ME, Langeveld JP, Smits MA (2000) Pathogenesis of natural scrapie in sheep. Arch Virol Suppl 16:57–71

21. van Keulen LJM, Schreuder BEC, Meloen RH, Mooij-Harkes G, Vromans MEW, Langeveld JPM (1996) Immunohistochemical detection of prion protein in lymphoid tissues of sheep with natural scrapie. J Clin Microbiol 34:1228–1231

22. van Keulen LJM, Vromans MEW, van Zijderveld FG (2002) Early and late pathogenesis of natural scrapie infection in sheep. Apmis 110:23–32

23. Wells GAH, Hawkins SAC, Green RB, Austin AR, Dexter I, Spencer YI, Chaplin MJ, Stack MJ, Dawson M (1998) Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. Vet Rec 142:103–106

24. Wells GAHH, Dawson M, Hawkins SAC, Green RB, Dexter I, Francis ME, Simmons MM, Austin AR, Horigan MW (1994) Infectivity in the ileum of cattle challenged orally with bovine spongiform encephalopathy. Vet Rec 135: 40–41

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However, in the absence of comprehensive infectivity data to facilitate a QRA, it was concluded that Specified Risk Materials (SRM) removal alone was unlikely to be sufficient to eliminate the residual BSE risk to the consumer from a BSE-infected sheep carcass.




Subject: OPINION, BSE RISK IN SHEEP, HOPING FOR THE BEST, PREPARING FOR THE WORST From: "Terry S. Singeltary Sr." <[log in to unmask]> Reply-To: Sustainable Agriculture Network Discussion Group <[log in to unmask]> Date: Fri, 16 Mar 2007 11:29:34 -0600




MADCOW USDA the untold story


Transmissible Mink Encephalopathy TME

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States


SEAC 99th meeting on Friday 14th December 2007


AS one of them _lay_ folks, one must only ponder ;

"WITH the Nor-98 now documented in five different states so far in the USA in 2007, and with the TWO atypical BSE H-BASE cases in Texas and Alabama, with both scrapie and CWD running rampant in the USA, IS there any concern from SEAC with the rise of sporadic CJD in the USA from ''UNKNOWN PHENOTYPE'', and what concerns if any, in relations to blood donations, surgery, optical, and dental, do you have with these unknown atypical phenotypes in both humans and animals in the USA ???"

"Does it concern SEAC, or is it of no concern to SEAC?"

"Should it concern USA animal and human health officials?"


----- Original Message ----- From: xxxxxxxxxx To: Sent: Thursday, November 22, 2007 5:39 AM Subject: QUESTION FOR SEAC

Mr Terry S Singeltary Sr., Bacliff, Texas 77518 USA.

Dear Mr Singeltary,

"Thank you for your e-mail of yesterday with the question for SEAC. I can confirm that this will be asked at the meeting on your behalf and the question and answer will appear in the minutes of the meeting which will be published on the SEAC Internet site."

snip...see full text ;


Saturday, December 08, 2007

SCRAPIE HB Parry Seriously’ (YB88/6.8/4.1)

Saturday, December 08, 2007 SCRAPIE HB Parry Seriously’ (YB88/6.8/4.1)

HB Parry Seriously’ (YB88/6.8/4.1)

IF the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease.

1: Neuroepidemiology. 1985;4(4):240-9.

Sheep consumption: a possible source of spongiform encephalopathy in humans.

Davanipour Z, Alter M, Sobel E, Callahan M.

A fatal spongiform encephalopathy of sheep and goats (scrapie) shares many characteristics with Creutzfeldt-Jakob disease (CJD), a similar dementing illness of humans. To investigate the possibility that CJD is acquired by ingestion of contaminated sheep products, we collected information on production, slaughtering practices, and marketing of sheep in Pennsylvania. The study revealed that sheep were usually marketed before central nervous system signs of scrapie are expected to appear; breeds known to be susceptible to the disease were the most common breeds raised in the area; sheep were imported from other states including those with a high frequency of scrapie; use of veterinary services on the sheep farms investigated and, hence, opportunities to detect the disease were limited; sheep producers in the area knew little about scrapie despite the fact that the disease has been reported in the area, and animal organs including sheep organs were sometimes included in processed food. Therefore, it was concluded that in Pennsylvania there are some 'weak links' through which scrapie-infected animals could contaminate human food, and that consumption of these foods could perhaps account for spongiform encephalopathy in humans. The weak links observed are probably not unique to Pennsylvania.

J Infect Dis 1980 Aug;142(2):205-8

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

PMID: 6997404





Nobel Lecture, December 13, 1976


National Institutes of Health, Bethesda, Maryland, U.S.A.


In a study in Israel, an

overall prevalence in Jews of Libyan origin is 30 times as high as in Jews of

European origin (40). The custom of eating the eyeballs and brains of sheep

in the Jewish households of North African and Middle Eastern origin, as opposed

to Jewish households of European origin, has understandably given rise to the

conjecture that scrapie-infected sheep tissue might be the source of such CJD

infection (37).


The passage of sheep scrapie into other sheep and into goats, at least by the

route of feeding of material contaminated with placenta and embryonic

membrane (53), and into mink from feeding carcasses of scrapied sheep, are

established paths of scrapie transmission. In view of the experimental transmission

of scrapie to monkeys, there is serious cause for wonder whether kitchen

and butchery accidents involving the contamination of skin and eyes may not

be a possible source of CJD in man (36a, 37).


Scrapie has been transmitted in our laboratory to five species of monkeys (Tables 9 and 10) (23, 31, 32), and such transmission has occurred using infected brain from naturally infected sheep and from experimentally infected goats and mice (Figures
22a, b, c). The disease produced is clinically and pathologically indistinguishable
from experimental CJD in these species. .........

Figure 22. Scrapie has been transmitted to three species of New World monkeys and two
species of Old World monkeys (Tables 9, 10). 22a. Transmission of scrapie from the brain of a scrapie-infected Suffolk ewe (C506) in Illinois to a cynomolgus monkey, and from the 4th mouse passage of this strain of scrapie virus to two squirrel monkeys. Incubation period in the cynomolgus was 73 months and in the squirrel monkeys 31 and 33 months. A chimpanzee and a rhesus monkey inoculated 109 months ago with this sheep brain remain well, as does a spider monkey inoculated 70 months ago with brain from the 4th passage of the C506 strain of scrapie in mice.


22b. Primary transmission of goat-adapted scrapie (Compton, England strain) to the
squirrel monkey and to mice and the transmission of mouse-adapted scrapie to two species of Old World and three species of New World monkeys. Numbers in parentheses are the number of months elapsed since inoculation, during which the animal remained asymptomatic.


22c. Transmission of mouse-adapted sheep scrapie (U. S. strain 434-3-897) to a squirrel monkey 38 months following intracerebral inoculation with a suspension of scrapie-infected mouse brain containing 10a7.3 infectious units of virus per ml. This animal showed signs of ataxia, tremors and incoordination, and the disease was confirmed histologically. See (b) for an explanation of symbols.


Figure 23. Transmissible mink encephalopathy (TME), a rare disease of American ranch
mink, is possibly a form of scrapie. The clinical picture and histopathological lesions attendant in the brain, resemble that of scrapie, and scrapie sheep carcasses were fed to mink on ranches on which TME appeared. The disease is transmissible to sheep, goats, certain rodents and New and Old World monkeys. Illustrative data on the primary transmissions of transmissible mink encephalopathy to one species of New World monkey and two species of Old World monkeys, and serial passage of the virus in squirrel, rhesus and stumptailed monkeys are presented in this Figure. Incubation periods are shown in months that elapsed between inoculation and onset of clinical disease. (Figure includes information from our laboratory and from R. F. Marsh, R. J. Eckroade, and R. P. Hanson.)

SNIP... end




Nobel Lecture, December 13, 1976


National Institutes of Health, Bethesda, Maryland, U.S.A.

Nature. 1972 Mar 10;236(5341):73-4.

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis). Gibbs CJ Jr, Gajdusek DC. ====================================

Proposed link between transmissible spongiform encephalopathies of man and animals.

Diringer H.

Robert Koch-Institut, Berlin, Germany.

A link between scrapie and Creutzfeldt-Jakob disease (CJD) is likely to exist. Based on old observations on scrapie, new experiments on bovine spongiform encephalopathy, and modern reviews on CJD, my proposal fits general rules of virus transmission

Additional Comments

63. I could perhaps sum up MAFF’s approach to BSE with an observation which is by no means original:

“Absence of evidence” is not the same as “evidence of absence”

“Absence of evidence” is not the same as “evidence of absence”

I think this might pertain to USDA et al on BSE, BASE, Scrapie's and the Nor-98, CWD, and TME, and human TSE therefrom. ...






Transmissible Mink Encephalopathy TME


Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States




Tuesday, December 04, 2007



Prepared by National Center for Animal Health Programs Ruminant Health Programs Team November 15, 2007


Infected and Source Flocks

During FY 2007, there were a total of 76 new infected or source flocks identified. Of those new flocks identified, 30 were infected flocks and 46 were source flocks (Figure 2). As of September 30, 2007, there were 38 scrapie infected and source flocks with open statuses (Figure 3). ...


In FY 2007, 331 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), including 59* Regulatory Scrapie Slaughter Surveillance (RSSS) cases (Figure 5 and Slide 16). In FY 2007, two field cases, one validation case, and two RSSS cases were consistent with Nor-98 scrapie. The Nor98-like cases originated from flocks in California, Minnesota, Colorado, Wyoming and Indiana respectively. Nineteen cases of scrapie in goats have been reported since 1990 (Figure 6). The last goat case was reported in September 2007.


see full report here ;


Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E11National Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway

Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was firstdescribed in Norway in 1998. Several features of Nor98 were shown to be differentfrom classical scrapie including the distribution of disease associated prion protein(PrPd) accumulation in the brain. The cerebellum is generally the most affected brainarea in Nor98. The study here presented aimed at adding information on theneuropathology in the cerebellum of Nor98 naturally affected sheep of variousgenotypes in Sweden and Norway. A panel of histochemical and immunohistochemical(IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein,amyloid, and cell markers for phagocytic cells were conducted. The type of histologicallesions and tissue reactions were evaluated. The types of PrPd deposition werecharacterized. The cerebellar cortex was regularly affected, even though there was avariation in the severity of the lesions from case to case. Neuropil vacuolation wasmore marked in the molecular layer, but affected also the granular cell layer. There wasa loss of granule cells. Punctate deposition of PrPd was characteristic. It wasmorphologically and in distribution identical with that of synaptophysin, suggestingthat PrPd accumulates in the synaptic structures. PrPd was also observed in thegranule cell layer and in the white matter. The pathology features of Nor98 in thecerebellum of the affected sheep showed similarities with those of sporadicCreutzfeldt-Jakob disease in humans.


typical scrapie transmits to primates by there NON-FORCED ORAL CONSUMPTION ;


full text ;


Transmissible Mink Encephalopathy TME


Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease inthe United States

i am reminded of a few things deep throat (high ranking official at usda)told me years ago;


The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people.........Dear God,