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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, January 30, 2012

The First Report of a Patient with Probable Variant Creutzfeldt-Jakob Disease in Turkey

Dement Geriatr Cogn Dis Extra. 2011 Jan-Dec; 1(1): 429–432. Published online 2011 December 24. doi: 10.1159/000332024 PMCID: PMC3265806

Copyright© 2011 by S. Karger AG, Basel

The First Report of a Patient with Probable Variant Creutzfeldt-Jakob Disease in Turkey

Demet Özbabalık Adapınar,a* Suzan Saylısoy,b Çınar Yenilmez,c Hüseyin Aslan,d Bengü Ertan,a Sevilhan Artan,d Gülcan Güleç,c Çiğdem Susuz,a and Baki Adapınarb

aDepartment of Neurology, Eskisehir Osmangazi University Medical Faculty, Eskisehir, Turkey

bDepartment of Radiology, Eskisehir Osmangazi University Medical Faculty, Eskisehir, Turkey

cDepartment of Psychiatry, Eskisehir Osmangazi University Medical Faculty, Eskisehir, Turkey

dDepartment of Medical Genetics, Eskisehir Osmangazi University Medical Faculty, Eskisehir, Turkey

*Demet Özbabalık Adapınar, Eskisehir Osmangazi University, TR–26480 Meselik/Eskisehir (Turkey), E-Mail

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial-No-Derivative-Works License ( Users may download, print and share this work on the Internet for noncommercial purposes only, provided the original work is properly cited, and a link to the original work on and the terms of this license are included in any shared versions.


Variant Creutzfeldt-Jakob disease (vCJD) was first reported in the UK in 1996. Here, we report the first Turkish case of vCJD. A 47-year-old man, who has never lived outside of Turkey and had had no transfusion, was admitted to the University Hospital with speech disorder, cognitive decline and ataxia following depression, irritability, and personality change. The immunoassay of the 14-3-3 protein in the cerebrospinal fluid was negative. Brain magnetic resonance imaging revealed high-signal lesions involving the bilateral caudate and lentiform nucleus on T2- and diffusion-weighted imaging. The patient developed akinetic mutism 10 months after disease onset. The clinical presentation and neuroimaging findings were compatible with the vCJD cases reported since 1996 and met the World Health Organization's case definition for probable vCJD.Key Words: Magnetic resonance imaging, Prion, Variant Creutzfeldt-Jakob disease

Other Sections▼ Abstract Introduction Case Report Discussion References


Creutzfeldt-Jakob disease (CJD), which is characterized by progressive dementia with a fatal and incurable course, is the most common human prion disease. There are 4 types of this disease: the sporadic (85%), familial (10–15%), iatrogenic (1%), and variant types [1]. Variant Creutzfeldt-Jakob disease (vCJD) was first reported in 1996 in the United Kingdom and has been causally linked to the consumption of cattle products contaminated with the bovine spongiform encephalopathy (BSE) agent [2]. To date, more than 215 cases of vCJD have been identified worldwide, including in the UK, France, Ireland, Italy, the USA, Canada, Saudi Arabia, Japan, The Netherlands, Portugal, Spain, and Taiwan. In the present paper, we report the clinical and radiological data of the first Turkish case of vCJD.

Other Sections▼ Abstract Introduction Case Report Discussion References

Case Report

A 47-year-old man, who was previously healthy and had no history of psychiatric or neurological disorders before the onset of this disease, presented with a 6-month history of progressive behavioral and personality changes, depression, and cognitive decline. His relatives reported that personality changes were his first symptoms. He had been a rigorous, disciplined, and frugal person, who was dependable at work and a valued member of his family; however, he became aggressive, extravagant, foul-mouthed, sexually disinhibited, and angry. His wife reported that the patient would have sudden outbursts of agitation, and 2 months later, these outbursts were followed by paranoid behaviors and possessiveness. Due to the psychiatric nature of his complaints, he was admitted to a psychiatry clinic, where he was diagnosed as having a manic disorder and was given atypical antipsychotic drugs. Three months later, the patient exhibited gait changes, ataxia and dysarthria, severe forgetfulness, difficulties in swallowing and eating, and incontinence. The patient developed involuntary movements in both of his feet, with dystonic aversion-inversion posturing and occasional erratic movements. He became dependent and apathetic and exhibited regressive behaviors. The patient also exhibited visual hallucinations, during which he reported seeing animals. Some of these complaints may have been side effects from his medication and, consequently, several of the patient's medications were stopped or changed.

As a result of the progressive deterioration of the patient's general status, his relatives transferred him to the Psychiatry Department of our University Hospital. After the neurological examination conducted at the Psychiatry Clinic, he was diagnosed as having rapid progressive dementia with early onset and was hospitalized at the Neurology Clinic. As reported in the patient's medical history, he had never been exposed to cadaveric pituitary hormones, had never undergone a neurosurgical procedure, organ or tissue grafts, or a blood transfusion, and had never travelled to the UK or to any country with reported incidences of BSE.

The neurological examination revealed that the patient was disorientated in place and time. In addition, he was mute. Nystagmus and conjugate gaze dysfunction were present, as were cerebellar ataxia, dysmetria, and dysdiadochokinesia. The patient's tone was slightly increased in his lower limbs, and his plantar responses were extensor.

The level of protein in his cerebrospinal fluid was increased, and no 14-3-3 protein was detected. An electroencephalogram showed a generalized slowing of wave, which was more evident in the left hemisphere, but did not have any periodic complexes. He was referred to the Radiology Department for cerebral MRI. On T2-weighted images and fluid-attenuated inversion recovery (FLAIR) images, hyperintense signal changes in the bilateral caudate nuclei (white arrows) and the lentiform nucleus (black arrows) were seen. In addition, hyperintensity in the bilateral thalamic region was less prominent than in the previously described areas (fig. 1a–c). Cortical hyperintensity was noted on diffusion-weighted imaging.

Fig. 1 MRI shows hyperintensity in the bilateral caudate (white arrows) and bilateral lentiform nucleus (black arrows) as well as in the bilateral thalamus (curved arrow) on axial T2-weighted image (a) and coronal FLAIR image (b). Ribbon-shaped hyperintense (more ...)

Genotyping of the prion protein gene (PRNP) identified a P102L mutation and heterozygosity for methionine at codon 129.The patient did not want to undergo a brain biopsy, and we continued to follow his progress at his home. At the time this report was written, the patient was alive, mute, and on bed rest. Other Sections▼ Abstract Introduction Case Report Discussion References


The patient described in the present report was the first probable case of vCJD in Turkey. The clinical features of this patient are consistent with the vCJD cases that have been identified in the UK and France, including psychiatric manifestations at the disease onset, a delayed occurrence of neurological signs, ataxia, and dementia [3]. In addition to the pulvinar sign that was present on the MRI and EEG, the patient fulfilled the WHO case definition for probable vCJD, the specificity of which is 100% [4]. Of note, a tonsil biopsy is not necessary if the clinical features and the MRI findings are compatible with vCJD, as the pulvinar sign is highly characteristic [5].

Sequencing analysis revealed that the patient had two different nucleotide changes in the coding region of the PRNP gene. The first one is the M129V polymorphism, and our patient was heterozygous for this alteration. Interestingly, all the patients who have undergone genotyping up to now have been homozygous for methionine at codon 129. This polymorphism is associated with susceptibility to prion diseases [6]. The second one is the P102L mutation, which was first identified in affected members of two unrelated families with Gerstmann-Sträussler disease. P102L is one of the most common PRNP mutations and also related to CJD.

This case highlights the difficulties in achieving an early diagnosis of vCJD. At the initial presentation, a variety of diagnoses were proposed, but vCJD was not considered in this patient. Instead, he was diagnosed as having an affective disorder at the psychiatry clinic. The delayed neurological signs in this patient pointed to the possibility of progressive dementia, which is not surprising given the frequency of psychiatric features that are observed by primary care physicians. These clinical features are often misleading. Almost half of the cases of vCJD were reviewed by a psychiatrist prior to the patients’ neurological referral [7]. A neurological etiology was usually suspected promptly after the patients developed objective neurological features, which resulted in a neurological referral in all of the cases. The single most important determinant of early diagnosis was the presence of objective neurological features. For this reason, all physicians must be careful when diagnosing rapidly progressing dementia that begins at a young age.

The results presented in this report indicate that patients with vCJD are still seen in the medical community. In the present study, we have reported the first Turkish vCJD case, which appeared 15 years after the first case in the UK.

Other Sections▼ Abstract Introduction Case Report Discussion References


1. Johnson RT. Prion diseases. Lancet Neurol. 2005;4:635–642.[PubMed]

2. Will RG, Ironside JW, Zeidler M, Cousens SN, Estibeiro K, Alperovitch A, Poser S, Pocchiari M, Hofman A, Smith PG. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet. 1996;347:92.[PubMed]

3. Brandel JP, Heath CA, Head MW, Levavasseur E, Knight R, Laplanche JL, Langeveld JP, Ironside JW, Hauw JJ, Mackenzie J, Alpérovitch A, Will RG, Haïk S. Variant CJD in France and the United Kingdom: evidence for the same agent strain. Ann Neurol. 2009;65:233–235. [PMC free article][PubMed]

4. World Health Organization: The revision of the surveillance case definition for variant Creutzfeldt-Jakob disease (vCJD). WHO/CDS/CSR/EPH/2001.5, 2002. Report of a WHO consultation.

5. Collie DA, Summers DM, Sellar RJ, Ironside JW, Cooper S, Zeidler M, Knight R, Will RG. Diagnosing variant Creutzfeldt-Jakob disease with the pulvinar sign: MR imaging findings in 86 neuropathologically confirmed cases. Am J Neuroradiol. 2003;24:1560–1569.[PubMed]

6. Lukic A, Beck J, Joiner S, Fearnley J, Sturman S, Brandner S, Wadsworth JD, Collinge J, Mead S. Heterozygosity at polymorphic codon 219 in variant Creutzfeldt-Jakob disease. Arch Neurol. 2010;67:1021–1023.[PubMed]

7. Lépine J, Gastpar M, Mendlwicz J, Tylee A. Depression in the community: the first pan-European study DEPRES (Depression Research in European Society. Int Clin Psychopharmacol. 1997;12:19–29.[PubMed]

European Journal of Human Genetics (2001) 2001 Nature Publishing Group

Distribution of the M129V polymorphism of the prion protein gene in a Turkish population suggests a high risk for Creutzfeldt-Jakob disease

Nihan Erginel-Unaltuna1, Katell Peoc'h2, Evrim Komurcu1, Tufan Tevfik Acuner3, Halim Issever4 and Jean-Louis Laplanche*,2 1Department of Genetics, Institute for Experimental Medical Research, Istanbul University, Istanbul, Turkey; 2Service de Biochimie et Biologie MoleÂculaire, Association Claude Bernard, HoÃpital LariboisieÁre, Paris, France; 33rd Neurology Clinic, Turkish Ministry of Health Bakirkoy Hospital for Psychiatric and Neurological Diseases, Istanbul, Turkey; 4Division of Biostatistics and Demography, Department of Public Health, Istanbul Medical School, Istanbul University, Istanbul, Turkey

A polymorphism (M129V) at codon 129 of the prion protein gene (PRNP) results in either a methionine residue (Met) or a valine residue (Val) and is known to determine susceptibility for the development of sporadic or acquired Creutzfeldt-Jakob disease (CJD). The distributions of M129V genotypes and alleles in various general populations have been reported and there are clear differences between Western Europeans and East Asians. We analysed the coding sequence of the PRNP gene in 100 healthy Turkish subjects to determine whether the distributions of the M129V genotypes and alleles or other PRNP gene variants in the Turkish population differ from those in other normal populations. Three known polymorphisms but no other gene variants were detected in the PRNP coding sequence of the Turkish individuals. Genotype frequencies at codon 129 were 57% Met/Met, 34% Met/Val and 9% Val/Val, with an allele frequency of 0.740 : 0.260 Met:Val. These distributions are considerably different from those reported for other normal populations residing in Western Europe and East Asia, except in Crete. The higher frequency of 129 Met-homozygotes in Turkey than in Western Europe suggests that the Turkish are at greater risk of developing CJD. European Journal of Human Genetics (2001) 9, 965 ± 968.

Keywords: Creutzfeldt-Jakob disease; prion; gene; PRNP; polymorphism; Turkey; population; genetic


Consequently, the distributions of the M129V genotypes and alleles in the Turkish population differ considerably from those reported for other normal populations residing in either Western Europe or East Asia, with the notable exception of Cretan natives. A recent report19 found that the high rate of PRNP 129Met homozygosity in Crete was associated with a local increase in the incidence of sporadic CJD. As homozygosity at PRNP codon 129 is a recognized risk factor for sporadic and acquired CJD in Caucasians5,21 and heterozygosity is protective,2 ± 4,21 the higher frequency of 129Met-homozygotes in Turkey than in Western Europe would also suggest that the Turkish are at increased risk of developing CJD.

see full report ;

Prp Gene Based Scrapie Susceptibility in Native Turkish Sheep: Do We Need To Introduce a Breeding Program to Select For Resistance to Scrapie in Turkey?

Emel OZKAN*, M. İhsan SOYSAL, Begüm UZUN, Ebru GOKALP, İnci TOGAN

Two studies on scrapie in Turkey (published)

“ Although not commented on in the Report, it is intriguing that the sampled Turkish population has the second highest polymorphic frequency of 129V (0.48), which is close to the that of the Fore population (0.55), and even closer to the expected equilibrium frequency of 0.45 (1). Given that there are no records of cannibalism in Turkish history, and the impossibility of the existence of undetected cannibalism of the scale observed in the Fore, there must be a different explanation for this high frequency. Sheep and cow brains are delicacies in Turkey, and certain popular restaurants (kelle pa�a) specialize in sheep brains and heads. The brains of sheep, cattle, pigs, primates, and other mammals are esteemed dietary items by people in many parts of the world, including the Middle East; north and central Africa; some Caribbean islands; central, south, and southeast Asia; “

Prion diseases and a penchant for brains

CONTRIBUTORS: Author: Sekercioglu, Cagan H. (Stanford University) JOURNAL: Science, 305(5682), 342 - 343. YEAR: 2004 PUB TYPE: Journal Article SUBJECT(S): Prions, kuru, Fore, Turks, cannibalism, scrapie, mad-cow disease, kelle pa�a, kokore�, balancing selection, epidemics, bovine spongiform encephalopathy, BSE, Creutzfeldt-Jakob disease, vCJD, brain consumption, public health DISCIPLINE: Medicine HTTP: LANGUAGE: English PUB ID: 103-405-161 (Last edited on 2004/07/20 18:41:32 GMT-6) SPONSOR(S):


In their Report "Balancing selection at the prion protein gene consistent with prehistoric kurulike epidemics," S. Mead et al. provide an interesting and persuasive argument on how kuru transmitted by endocannibalism resulted in balancing selection at codon 129 of human prion protein gene in the Fore linguistic group of Papua New Guinea (25 Apr. 2003, p. 640). I am not convinced, however, that acquired prion disease causing the selective pressure results mainly from cannibalism in other populations around the world. Although not commented on in the Report, it is intriguing that the sampled Turkish population has the second highest polymorphic frequency of 129V (0.48), which is close to the that of the Fore population (0.55), and even closer to the expected equilibrium frequency of 0.45 (1). Given that there are no records of cannibalism in Turkish history, and the impossibility of the existence of undetected cannibalism of the scale observed in the Fore, there must be a different explanation for this high frequency. Sheep and cow brains are delicacies in Turkey, and certain popular restaurants (kelle pa�a) specialize in sheep brains and heads. The brains of sheep, cattle, pigs, primates, and other mammals are esteemed dietary items by people in many parts of the world, including the Middle East; north and central Africa; some Caribbean islands; central, south, and southeast Asia; Russia; Iceland; southern Europe; and North and Latin America. In Mead et al.'s Table 1, the samples from many of these groups also show relatively high M129V frequencies. In cases of bovine spongiform encephalopathy (BSE) and scrapie, prion diseases found in cattle and sheep, the prions are concentrated in the brain and other nervous tissues (2), and the high frequency of M129V in many groups can also be explained by regular exposure to prion diseases as a result of frequent consumption of animal brains. Even though Mead et al. mention the possibility of animal prion disease as an explanation for the observed pattern, they clearly favor cannibalism as the main cause, citing the evidence for prehistoric cannibalism in certain human populations. However, variant Creutzfeldt-Jakob disease (vCJD) has been transmitted from BSE-infected cattle to humans (3); the BSE agent can infect various animals (such as cattle, goats, pigs, and sheep) that are often consumed by people (4); the significant increase in vCJD incidence in Leicestershire, England, was a result of the contamination of cow meat with central nervous system tissue (2); the high incidence of CJD in Libyan Jews (5) and Slovakian herdsmen (6) correlates with a high preference for sheep brains; and in rural Kentucky, a fondness for squirrel brains suggests a similar connection (7). An important reason for the dietary preference for brain tissue is its high fat content. This can also be seen in wild chimpanzees feeding on monkeys (8), and it is likely to have been present in prehistoric human populations feeding on a diversity of animals. That 85% of human transmissible spongiform encephalopathies are sporadic and have no known etiologies (2); that many people regularly consume ruminant intestinal tissue, which also has a high concentration of BSE prions (9); and that other possible vectors of human prion diseases include rodents (10) and flies (11) necessitate further caution in assigning cannibalism as the predominant cause of balancing selection at the prion protein gene in human populations worldwide. Prion diseases in people, especially outside the developed world, are likely to be misdiagnosed and underrecorded. To the extent possible, consumption of mammal brains, intestines, and other highly infective tissue should be evaluated as a potential causal factor in any study of human prion diseases.

-------- Original Message --------


Date: Wed, 31 Mar 2004 10:01:26 –0600

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy


######## Bovine Spongiform Encephalopathy #########


A SEARCH FOR THE MODE OF NATURAL TRANSMISSION1 Harvey Goldberg2, Milton Alter3, and Esther Kahana4 ABSTRACT In 1974, we reported chat Creutzfeldt-Jakob disease (CJD), a fatal slow virus disease of man, occurred at least thirty tines more commonly In Libyan Jewish immigrants to Israel than all other groups studied. The mode of natural transmission of CJD Is unknown. This report describes genetic and environ- mental factors Investigated In an effort to explain the focus of CJD among Libyan Jews. A total-of 14 Libyan and 11 non-Libyan cases of CJD were studied. Of these, three were diagnosed after completion of our original report and two In the original report did not participate in this study. Among the 14 Libyans with CJD diagnosed between 1963 and 1974 and available for this study, two definite and three possible familial cases were identi- fied. Parents were first cousins in three of 14 (21%) cases among the Libyans, but 18% of a control sample of Tunisians also report first cousin marriages between parents. Non-Libyan patients had no familial cases but the holocaust and dispersion of families made collection of reliable pedigrees difficult. Because CJD can be transmitted experimentally by inoculation of susceptible animals with brain tissue, dietary habits were investi- gated. Over 80% of Libyan patients ate brain but they did not appear to differ in this respect from controls. Libyan cases resembled controls also In source of meat and frequency of meat consumption. However, Libyan Jews preferred quick-grilled brain while Tunisians preferred fried and simmered brain. In their occupations, Libyans 1This work was supported In part by grants from the National Institutes of Health (NS13766-02) and from the Medical Research Council of Israel. 2Department of Sociology and Social Anthropology, Hebrew University of Jerusalem, Jerusalem, Israel. 3Department of Neurology, Temple University, School of Medicine, 3401 N. Broad Street, Philadelphia. PA 19140. 4Uri Leibowicz Neuroepidemiology Unit, Department of Neurology, Hadassah Hebrew University Hospital, Jerusalem, Isr snip...

Harvey Golberg et al.

regularly by residents of rural towns; the rural population ate goat as well. Chicken was eaten frequently by everyone, turkey much less frequently. There was no systematic differ- ence among the patients and the three control groups in the type of meat eaten or in the frequency of meat consumption.

Table 3 contains more detailed information on the con- sumption of brain. The percentages of those eating brain sometimes ranged from 79 to 92 for the four groups. The patient group was not consistently higher than any of the control groups. A higher percentage of Libyans ate brain in our small sample than in Bobowick's series (8). The percent- age eating spinal cord was consistently lower than that of brain consumers, but many people said that some spinal cord may have been found in bones purchased for soup, and the actual consumption of spinal cord may have been higher than that shown in Table 3.

Brain was commonly prepared in stew (m'chuma) and in a patty (m'akod). The number of people who reported eating these dishes at least once every two months was low (10-25%), and was not different in patients compared to controls.

Brain was also prepared by grilling, typically while the brain was wrapped in heavy paper, so that the full effect of the heat did not reach the brain. Usually the grilling was for a brief period of time, often less than five minutes. The number of people who reported eating grilled brain which was on the fire less than twenty minutes is shown in Table 3. More than one-third of the patients were described as having eaten brain prepared in this manner, but each of the control groups reported a higher precentage.

The Libyans also reported eating eyeballs, although not with great frequency. This question was introduced midway through the research so that only some people were queried. The small number of cases interviewed did not suggest any difference between patients and controls.

Reviewing the dietary data presented in Tables 2 and 3, it appears that meat consumption was relatively high among Libyan Jews, that brain was eaten by most people at some time, and that brain was eaten by many people several times a year. Patients, however, did not appear different from controls in most of the variables studied. Thus, there is an overall consistency in the answers among the four groups of Libyan respondents. While this was encouraging so far as the quality of the data is concerned, it did not support the hypothesis that (diseased) brain consumption set patients apart from other Libyans. It is still conceivable that high consumption of brain places the Libyan population at high risk with regard to CJD, but that another mechanism, perhaps genetic, makes some individuals more vulnerable than others...



1: Eur J Epidemiol 1991 Sep;7(5):520-3

"Clusters" of CJD in Slovakia: the first laboratory evidence of scrapie.

Mitrova E, Huncaga S, Hocman G, Nyitrayova O, Tatara M.

Institute of Preventive and Clinical Medicine, Bratislava.

Epidemic-like occurrence of Creutzfeldt-Jakob disease was observed in 1987 in Slovakia (Orava). Search for the cause of CJD focus indicated a coincidence of genetic and environmental risks in clustering patients. Since Spongiform Encephalopathies might be transmitted orally, (Bovine Spongiform Encephalopathy), the possibility of zoonotic source of CJD cases in Orava was also considered. A deficient knowledge about the occurrence of scrapie in Slovakia stimulated an examination of sheep with signs of CNS disorders in two flocks of Valasky breed in Orava. In one flock, neurohistopathological examination revealed in sheep brains lesions characteristic for scrapie. Frozen brain tissue of these animals were used for the detection of scrapie associated fibrils. They were found in 2 animals from the same flock. This is the first laboratory confirmation of scrapie in Czecho-Slovakia. The possible epidemiological and economical implications are emphasized.

Scrapie to Humans USA?

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

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.

PMID: 3915057 [PubMed - indexed for MEDLINE]




IF THERE is one categorical pronouncement you can safely make about prion diseases like BSE or CJD, it is that one should not make categorical pronouncements. "British beef is safe" and "there is no BSE in Germany" come to mind. Now there are two more: "scrapie is safe", and "people don't catch sporadic CJD". Scrapie is the most widespread prion disease, infecting untold numbers of sheep worldwide. Sporadic CJD is the old-fashioned pre-BSE kind that is supposed to happen spontaneously in unlucky people. But a surprise observation in France suggests some sCJD cases--though by no means all--may be linked to scrapie after all (see p 4).

For years, British authorities asserted that BSE was harmless because it was a form of scrapie. In fact, the only evidence scrapie is safe is some broad-brush epidemiology, good as far as it goes but unable to reveal occasional risks for some people from some sheep. Alarm bells should have rung in 1980 when researchers gave monkeys scrapie by feeding them infected brains. But that research, like so much other work on prion diseases, was never followed up. We still have little idea what BSE does in pigs and chickens. The Queniborough vCJD outbreak (see p 5) would be easier to understand if we knew how much brain we must eat to be infected. As for scrapie, it shouldn't take a chance finding to tell us that there may be dangerous sheep out there.

Suspect symptoms

What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?

28 Mar 01

Like lambs to the slaughter

31 March 2001

by Debora MacKenzie

Magazine issue 2284.

FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.

Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.

Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.

"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.

Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.

Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.

As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.

"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.

But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.

People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.

But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."

There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.

Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.

“The agent responsible for French iatrogenic growth hormone-linked CJD taken as a control is very different from vCJD but is similar to that found in one case of sporadic CJD and one sheep scrapie isolate.”

Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt– Jakob disease: Implications for human health

Corinne Ida Lasmézas*†, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp‡, Jean-Jacques Hauw§, James Ironside¶, Moira Bruce‖, Dominique Dormont*, and Jean-Philippe Deslys*

+ Author Affiliations

*Commissariat à l'Energie Atomique, Service de Neurovirologie, Direction des Sciences du Vivant/Département de Recherche Medicale, Centre de Recherches du Service de Santé des Armées 60-68, Avenue du Général Leclerc, BP 6, 92 265 Fontenay-aux-Roses Cedex, France; ‡Hôpital Neurologique Pierre Wertheimer, 59, Boulevard Pinel, 69003 Lyon, France; §Laboratoire de Neuropathologie, Hôpital de la Salpêtrière, 83, Boulevard de l'Hôpital, 75013 Paris, France; ¶Creutzfeldt–Jakob Disease Surveillance Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom; and ‖Institute for Animal Health, Neuropathogenesis Unit, West Mains Road, Edinburgh EH9 3JF, United Kingdom

Edited by D. Carleton Gajdusek, Centre National de la Recherche Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000 (received for review October 16, 2000)


There is substantial scientific evidence to support the notion that bovine spongiform encephalopathy (BSE) has contaminated human beings, causing variant Creutzfeldt–Jakob disease (vCJD). This disease has raised concerns about the possibility of an iatrogenic secondary transmission to humans, because the biological properties of the primate-adapted BSE agent are unknown. We show that (i) BSE can be transmitted from primate to primate by intravenous route in 25 months, and (ii) an iatrogenic transmission of vCJD to humans could be readily recognized pathologically, whether it occurs by the central or peripheral route. Strain typing in mice demonstrates that the BSE agent adapts to macaques in the same way as it does to humans and confirms that the BSE agent is responsible for vCJD not only in the United Kingdom but also in France. The agent responsible for French iatrogenic growth hormone-linked CJD taken as a control is very different from vCJD but is similar to that found in one case of sporadic CJD and one sheep scrapie isolate. These data will be key in identifying the origin of human cases of prion disease, including accidental vCJD transmission, and could provide bases for vCJD risk assessment.


1: 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.


The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

PMID: 6997404





A The Present Position with respect to Scrapie A] The Problem Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries. The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep. It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible. Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates.

One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias" Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.



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

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

C. J. GIBBS jun. & D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

Wednesday, February 16, 2011




Sunday, April 18, 2010


Monday, April 25, 2011

Experimental Oral Transmission of Atypical Scrapie to Sheep

Volume 17, Number 5-May 2011

Wednesday, January 18, 2012


February 1, 2012

Wednesday, January 18, 2012

Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural Scrapie Isolates Similar to CH1641 Experimental Scrapie

Journal of Neuropathology & Experimental Neurology:

February 2012 - Volume 71 - Issue 2 - p 140–147

Thursday, July 14, 2011

Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)

Monday, June 27, 2011

Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease

Wednesday, January 11, 2012

Bucks for brains on offer to cattle and sheep producers Queensland TSE PRION TESTING


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. ...

Thursday, November 18, 2010

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

Sunday, December 12, 2010

EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010

Monday, November 22, 2010

Atypical transmissible spongiform encephalopathies in ruminants: a challenge for disease surveillance and control


Wednesday, January 19, 2011

EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011


Prion Disease Risks in the 21st Century 2011

PDA European Virus-TSE Safety Dr. Detwiler

Dr. Detwiler published Prion Disease Risks in the 21st Century 2011 PDA European Virus-TSE Safety Forum\Presentations TSE\ Page 33 and 34 of 44 ;

Thursday, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659


*** UPDATE MARCH 20, 2012 ***

-----Original Message-----

From: Terry S. Singeltary Sr.

Sent: Tuesday, March 20, 2012 12:14 PM


Subject: Re: [CJD-L] The First Report of a Patient with Probable Variant Creutzfeldt-Jakob Disease in Turkey

IN reply to ;

Response to the Article by Adanipar et al.:

The First Report of a Patient with Probable Variant Creutzfeldt-Jakob Disease in Turkey, Dement Geriatr Cogn Disord Extra 2011;1:429–432

Dear Editor

It is essential that all cases of variant Creutzfeldt-Jakob disease (vCJD) are reported as the incidence and geographic distribution of cases inform public health policy. Validated criteria for the classification of cases of suspected vCJD [1] have been agreed on internationally and contain obligatory preconditions, the presence of specific clinical features, and the results of specialist investigations, including the ‘pulvinar sign’ on MRI brain scan. A definitive diagnosis of vCJD requires neuropathological confirmation, either at brain biopsy or autopsy.

The case described by Adanipar et al. [2] has been reported as a case of ‘probable variant Creutzfeldt-Jakob disease’. However, although the clinical features would be compatible with this condition, other characteristics of the case make this diagnosis unlikely. One of the preconditions for the diagnosis of vCJD is that there should be ‘no evidence of a familial form of TSE’, but the authors have identified a P102L mutation, an abnormality associated with the familial prion disease Gerstmann-Straussler disease [3] . The codon 129 genotype was heterozygous, which has not been identified, to date, in any definite or probable case of vCJD. The MRI scan images published in the article show high signal in the caudate and lentiform nuclei, appearances seen in sporadic CJD [4] , and not the ‘pulvinar sign’ which is characteristic of vCJD.

The case reported is of significant interest, but the suggested diagnosis of vCJD cannot be regarded as correct unless there is neuropathological verification of this diagnosis.

Yours sincerely,


R.G. Will This is an Open Access article licensed under the terms of the Creative Commons Attribution- NonCommercial-NoDerivs 3.0 License (, applicable to the online version of the article only. Distribution for non-commercial purposes only. National CJD Research and Surveillance Unit, Western General Hospital Edinburgh EH4 2XU (UK) Tel. +44 131 537 2085, E-Mail DOI: 10.1159/000337504

References 1 Heath CA, Cooper SA, Murray K, Lowman A, Henry C, Macleod MA, Stewart GE, Zeidler M, Mackenzie JM, Ironside JW, Summers DM, Knight RS, Will RG: Validation of diagnostic criteria for variant Creutzfeldt-Jakob disease. Ann Neurol 2010; 67: 761–770. 2 Adapınar DÖ, Saylısoy S, Yenilmez Ç, Aslan H, Ertan B, Artan S, Güleç G, Susuz Ç, Adapınar B: The first report of a patient with probable variant Creutzfeldt-Jakob disease in Turkey. Dement Geriatr Cogn Disord Extra 2011; 1: 429–432. 3 Kovacs GG, Trabattoni G, Hainfellner JA, Ironside JW, Knight RSG, Budka H: Mutations of the prion protein gene: phenotypic spectrum. J Neurol 2002; 249: 1567–1582. 4 Zerr I, Kallenberg K, Summers DM, Romero C, Taratuto A, Heinemenn U, Breithaupt M, Varges D, Meissner B, Ladogana A, Schuur M, Haik S, Collins SJ, Jansen GH, Stokin GB, Pimentel J, Hewer E, Collie D, Smith P, Roberts H, Brandel JP, van Duijn C, Pocchiari M, Begue C, Cras P, Will RG, Sanchez- Juan P: Updated clinical diagnostic criteria for sporadic Creutzfeldt-Jakob disease. Brain 2009; 132: 2659–2668.

I kindly submit the following;

THE UKBSEnvCJD only theory, is wrong, and only enhances the spread of other zoonosis strains of human and animal Transmissible Spongiform Encephalopathy TSE prion disease around the globe.

THE OIE and USDA stance on the BSE MRR policy, and disregard from their own science on atypical BSE, also, enhances the spread of human and animal Transmissible Spongiform Encephalopathy TSE prion disease around the globe.

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story


EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.


see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

Second threat


Rural and Regional Affairs and Transport References Committee

The possible impacts and consequences for public health, trade and agriculture of the Government's decision to relax import restrictions on beef Final report June 2010

2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49

2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50

snip...see full text and more here ;

Thursday, March 01, 2012

Variant Creutzfeldt-Jakob disease Fact sheet N°180 Revised February 2012 W.H.O.

***** Monday, March 19, 2012 *****

Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy

PLoS One. 2012; 7(2): e31449.

Friday, March 09, 2012

Experimental H-type and L-type bovine spongiform encephalopathy in cattle: observation of two clinical syndromes and diagnostic challenges

Research article

Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque

"BSE-L in North America may have existed for decades"

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.


The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...


Sunday, March 11, 2012

APHIS Proposes New Bovine Spongiform Encephalopathy Import Regulations in Line with International Animal Health Standards Proposal Aims to Ensure Health of the U.S. Beef Herd, Assist in Negotiations

Greetings USDA, OIE et al,

what a difference it makes with science, from one day to the next. i.e. that mad cow gold card the USA once held. up until that fateful day in December of 2003, the science of BSE was NO IMPORTS TO USA FROM BSE COUNTRY.

what a difference a day makes$ now that the shoe is on the other foot, the USDA via the OIE, wants to change science again, just for trade $

I implore the OIE decision and policy makers, for the sake of the world, to refuse any status quo of the USA BSE risk assessment. if at al, the USA BSE GBR should be raise to BSE GBR IV, for the following reasons.

North America is awash with many different TSE Prion strains, in many different species, and they are mutating and spreading.

IF the OIE, and whatever policy makers, do anything but raise the risk factor for BSE in North America, then I would regard that to be highly suspicious.

IN fact, it would be criminal in my opinion, because the OIE knows this, and to knowingly expose the rest of the world to this dangerous pathogen, would be ‘knowingly’ and ‘willfully’, just for the almighty dollar, once again.

I warned the OIE about all this, including the risk factors for CWD, and the fact that the zoonosis potential was great, way back in 2002.

THE OIE in collaboration with the USDA, made the legal trading of the atypical Nor-98 Scrapie a legal global commodity. yes, thanks to the OIE and the USDA et al, it’s now legal to trade the atypical Nor-98 Scrapie strain all around the globe. IF you let them, they will do the same thing with atypical BSE and CWD (both strains to date). This with science showing that indeed these TSE prion strains are transmissible.

I strenuously urge the OIE et al to refuse any weakening to the USA trade protocols for the BSE TSE prion disease (all strains), and urge them to reclassify the USA with BSE GBR IV risk factor.


Saturday, March 5, 2011


Sunday, February 12, 2012

National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas

DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)

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, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why????than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!! Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a is a big fat sponge...the agent continues to eat the brain can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....

Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any is ALL gonna be sporadic!!!

And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...

Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"

again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.

You need to watch your back........but keep picking at a buzzard to the just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)



Perceptions of unconventional slow virus in the USA


Report of a visit to the U.S.A. April-May 1989

3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed.

Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fantical incident to be avoided in the USA AT ALL COSTS.

Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009

re-Human Prion Diseases in the United States

Posted by flounder on 01 Jan 2010 at 18:11 GMT

I kindly disagree with your synopsis for the following reasons ;

Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***


Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2007.

Owens, Julie

From: Terry S. Singeltary Sr. []

Sent: Monday, July 24, 2006 1:09 PM To: FSIS RegulationsComments

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98 8/3/2006

Greetings FSIS, I would kindly like to comment on the following ;

Response to Public Comments on the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005


The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website:

Comments on technical aspects of the risk assessment were then submitted to FSIS.

Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.

This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:

Suppressed peer review of Harvard study October 31, 2002.

October 31, 2002 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report Prepared for U.S. Department of Agriculture Food Safety and Inspection Service Office of Public Health and Science Prepared by RTI Health, Social, and Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024

Sunday, February 14, 2010

[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)

Sunday, August 09, 2009

CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009

Tuesday, August 18, 2009

BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009

kind regards, terry


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518


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