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

Dear Dr. Singeltary,

According to our Information for Authors and Correspondence policy, we can only consider Correspondence written about articles published within the last six weeks. Please consider Neurology again in the future.

Sincerely,

Morgan Serry

Neurology Editorial Office

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VIEWS & REVIEWS: Ermias D. Belay, Ryan A. Maddox, Pierluigi Gambetti, and Lawrence B. Schonberger

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Neurology 2003; 60: 176-181 [Abstract] [Full text] [PDF]

Correspondence ID: neurology_el;17008

Article ID: 60/2/176 Article Date: 28 January 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 25 October 2007

http://www.neurology.org/cgi/eletters/60/2/176#535


I URGE you to consider my response once again. I think I have been proven correct now.

3 MONTHS LATER IN A BOOK INTERVIEW, VENDICATION OF SORTS

THE PATHOLOGICAL PROTEIN

Hardcover, 304 pages plus photos and illustrations.

ISBN 0-387-95508-9

June 2003

BY Philip Yam

CHAPTER 14 LAYING ODDS

Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded

that the current surveillance system has errors but stated that most of the errors will be confined to the older population.

http://www.thepathologicalprotein.com/


IN REALITY, sporadic CJD is 1 in 9,000 in 50 years of age and above, and that's with a inadequate or what I call passive surveillance system. see below ;

Dr. William Shulaw, a veterinarian with The Ohio State University extension service, is involved in a nationwide program to eradicate scrapie, the form of BSE found in sheep.

Shulaw said the chances of a person getting sporadic Creutzfeldt- Jakob disease is about one in a million. But that's the total population, infants, children, adults and the elderly. Chances increase to one in 9,000 when the group is restricted to those age 50 and older.

http://www.pjstar.com/stories/082207/REG_BE523NH6.049.php

2008 The statistical incidence of CJD cases in the United States has been revised to reflect that there is

_one case per 9000 in adults age 55 and older_.

Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

http://www.cjdfoundation.org/fact.html


FURTHER into my journal of neurology article, some years later, again, sadly, I was proven correct ;

SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ...

http://www.cjdsurveillance.com/resources-casereport.html


There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.

He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf


and today we indeed find ;

PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increase in ''TYPE UNKNOWN'' CJD IN THE USA ;

1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006, *** 26 from 2007)

http://www.cjdsurveillance.com/pdf/case-table.pdf


HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory

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 theUKBSEnvCJD only theory in 2007. With all the science to date refuting it, to continue to validate this myth, will only spread this TSE agent through a multitude of potential and proven routes and sources i.e. consumption, surgical, blood, medical, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub-clinical to clinical disease, and key to all this, is to stop the amplification and transmission of the TSE agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE (one strain TSE in cows), and the nv/v CJD (one strain TSE humans) and that all the rest of human TSE are just one single strain i.e. sporadic CJD (when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al), and that no other animal TSE transmits to humans, to continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. HeidenhainVariant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human.

With the H-BASE atypical BSE strain, and the Nor-98 atypical Scrapie strain, BOTH now documented in the USA, and BOTH more closely related pathologically to the sporadic CJD, rather than the BSE strain, I once again urge you to make all human TSE strains in the USA reportable in every state, and Internationally, with a written mandatory CJD/TSE questionnaire asking real questions pertaining to route and source of the TSE agent. This is paramount for iCJD i.e. friendly fire, and secondary transmissions via the medical, dental, and surgical arena alone.

WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...

flounder9@verizon.net

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

CJD NEWS

http://disc.server.com/Indices/236650.html


CJD VOICE (voice for _all_ victims of human TSE)

http://members.aol.com/larmstr853/cjdvoice/cjdvoice.htm


SOURCE

Subject: PRION2007 ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007 Date: September 24, 2007 at 6:52 pm PST

P02.35 Molecular Features of the Protease-resistant Prion Protein (PrPres) in H- type BSE

Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden

Western blot analyses of PrPres accumulating in the brain of BSE- infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H- type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C- terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) *** reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.

FC5.5.1 BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc C-terminal Truncated Fragments

Zanusso, G1; Commoy, E2; Fasoli, E3; Fiorini, M3; Lescoutra, N4; Ruchoux, MM4; Casalone, C5; Caramelli, M5; Ferrari, S3; Lasmezas, C6; Deslys, J-P4; Monaco, S3 1University of Verona, of Neurological and Visual Sciences, Italy; 2CEA, IMETI/SEPIA, France; 3University of Verona, Neurological and Visual Sciences, Italy; 4IMETI/SEPIA, France; 5IZSPLVA, Italy; 6The Scripps Research Insitute, USA

The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent human prion disease, remains still unknown. The marked disease phenotype heterogeneity observed in sCJD is thought to be influenced by the type of proteinase K- resistant prion protein, or PrPSc (type 1 or type 2 according to the electrophoretic mobility of the unglycosylated backbone), and by the host polymorphic Methionine/Valine (M/V) codon 129 of the PRNP. By using a two-dimensional gel electrophoresis (2D-PAGE) and imunoblotting we previously showed that in sCJD, in addition to the PrPSc type, distinct PrPSc C-terminal truncated fragments (CTFs) correlated with different sCJD subtypes. Based on the combination of CTFs and PrPSc type, we distinguished three PrPSc patterns: (i) the first was observed in sCJD with PrPSc type 1 of all genotypes,;

(ii) the second was found in M/M-2 (cortical form); (iii) the third in amyloidogenic M/V- 2 and V/V-2 subtypes (Zanusso et al., JBC 2004) . Recently, we showed that sCJD subtype M/V-2 shared molecular and pathological features with an atypical form of BSE, named BASE, thus suggesting a potential link between the two conditions. This connection was further confirmed after 2D-PAGE analysis, which showed an identical PrPSc signature, including the biochemical pattern of CTFs. To pursue this issue, we obtained brain homogenates from Cynomolgus macaques intracerebrally inoculated with brain homogenates from BASE. Samples were separated by using a twodimensional electrophoresis (2D-PAGE) followed by immunoblotting. We here show that the PrPSc pattern obtained in infected primates is identical to BASE and sCJD MV-2 subtype. *** These data strongly support the link, or at least a common ancestry, between a sCJD subtype and BASE. This work was supported by Neuroprion (FOOD-CT-2004-506579)

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USA MAD COW CASES IN ALABAMA AND TEXAS

***PLEASE NOTE***

USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet- mg&T=0&P=19779


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FC5.5.2 Transmission of Italian BSE and BASE Isolates in Cattle Results into a Typical BSE Phenotype and a Muscle Wasting Disease

Zanusso, G1; Lombardi, G2; Casalone, C3; D’Angelo, A4; Gelmetti, D2; Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini, M1; Gelati, M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1; Caramelli, M3; Capucci, L2 1University of Verona, Neurological and Visual Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA, Italy; 4University of Turin, Animal Pathology, Italy; 5Isituto Carlo Besta, Italy

The clinical phenotype of bovine spongiform encephalopathy has been extensively reported in early accounts of the disorder. Following the introduction of statutory active surveillance, almost all BSE cases have been diagnosed on a pathological/molecular basis, in a pre-symptomatic clinical stage. In recent years, the active surveillance system has uncovered atypical BSE cases, which are characterized by distinct conformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose clinicopathological phenotypes remain unknown. We recently reported two Italian atypical cases with a PrPSc type similar to BSE-L, pathologically characterized by PrP amyloid plaques. Experimental transmission to TgBov mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely virulent. A major limitation of transmission studies to mice is the lack of reliable information on clinical phenotype of BASE in its natural host. In the present study, we experimentally infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolates by i.c. route. BASE infected cattle showed survival times significantly shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with previous observations in TgBov mice. Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and in experimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness. The molecular and neuropathological profiles, including PrP deposition pattern, closely matched those observed in the original cases. This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle *** and in some subtypes of inherited and sporadic Creutzfeldt-Jakob disease. Oral Abstracts 14

P04.49

Case Report of Variant Creutzfeldt-Jakob Disease in a Macaque after Blood Transfusion

Lescoutra-Etchegaray, N1; Ruchoux, MM1; Correia, E1; Jolit, A1; Freire, S1; Lasmezas, CI2; Deslys, JP1; Comoy, E1 1CEA/DSV/IMETI/SEPIA, France; 2Scripps Florida, USA

A fourth human case of probable transmission of vCJD through transfusion has now been reported but a number of features affecting transfusion-related infection remain imprecise, including infectious dose, length of incubation period and critical infectious window of blood donors.

We report here the first case of experimental transmission of vCJD in primates by blood transfusion. Experimental infection of Cynomolgus macaque has been demonstrated to be a sensitive model for the investigation of human prion diseases, inducing similar distribution of infectivity in peripheral lymphoid tissues and equivalent brain pathology. In our study, transfusion was performed with 40 ml of whole blood drawn from a vCJD-infected macaque at the terminal stage of the disease. Clinical symptoms of vCJD appeared in the recipient animal after five years of incubation. The total amount of infectivity in the transfused blood was approximately 106 fold lower than in the brain (titration still in progress). In several animals infected intravenously with brain homogenate, the presence of PrPres in serial lymph nodes biopsies and in other organs at autopsy was examined and results will be presented.

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


P04.51

Atypical Presentation of Variant Creutzfeldt-Jakob Disease in a 73 Year Old Blood Transfusion Recipient

Wroe, S1; Pal, S1; Webb, T1; Alner, K2; Hewitt, P3; Brander, S4; Wadsworth, JD5; Collinge, J1 1National Hospital for Neurology and Neurosurgery, National Prion Clinic, UK; 2National Hospital for Neurology and Neurosurgery, Department of Neuropsychology, UK; 3Health Protection Agency, UK; 4National Hospital for Neurology and Neurosurgery, Department of Neuropathology, UK; 5Institute of Neurology, UCL, UK

We report atypical presentation of variant Creutzfeldt-Jakob Disease (vCJD) identified ante-mortem in a 73 year-old recipient of blood products. This patient was transfused following orthopaedic surgery in December 1997. Tracing of blood products identified a single unit of non-leucodepleted red cells from an individual who developed neuropathologically confirmed vCJD eleven months after donation. Nine years post transfusion, this individual was referred to the National Prion Clinic for specialist investigation. Six years post transfusion the recipient complained of fluctuating fatigue and impaired concentration. At this time neurological examination and MRI brain (T1/T2 weighted/DWI) were normal. Progressive symptoms emerged six months later with imbalance and deteriorating cognition. Examination two months after onset of neurological symptoms demonstrated cognitive deficits, dyspraxia or visuospatial dysfunction and normal motor, sensory and gait examination. Six weeks later cognitive impairment was identified alongside tremulousness, impaired manual dexterity and limb ataxia. Serological investigations were normal. MRI (T1/T2 weighted/FLAIR/DWI) demonstrated prominent signal change throughout the dorsal thalamus, consistent with vCJD. PRNP genotyping revealed no mutations and homozygosity for methionine at codon 129. The prolonged incubation period of vCJD and possibility of asymptomatic carrier states pose major public health concerns. This case highlights the significant risk encountered by recipients of contaminated blood products and the necessity for their specialist monitoring.

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


P04.36

Enhanced Surveillance of Persons Identified as at Increased Risk of CJD Due to Blood Transfusion or Healthcare Procedures

Brookes, D1; Chow, Y1; Ward, HJT2; Will, RG2; Hewitt, P3; Gill, ON1 1HPA, CJD, UK; 2National CJD Surveillance Unit, UK; 3Colindale, NHS Blood and Tissue, UK

Introduction:

Reports of four iatrogenic transmissions of variant-CJD (vCJD) infection in the UK (all due to transfusion of blood from donors who later developed vCJD), evidence from iatrogenic transmissions of sporadic CJD and experimental work on CJD infectivity in tissues and on healthcare instruments have given rise to concern about the risks of iatrogenic transmission of CJD. This risk warrants a) certain public health precautions, and b) follow-up of individuals with identified risks in order to gain evidence about their risks and ensure appropriate management of these risks. Evidence of transmission via iatrogenic routes is important to inform public health measures and so prevent ongoing transmission of CJD.

Methods:

The Health Protection Agency and Health Protection Scotland holds details of persons identified as ‘at-risk’ of vCJD due to blood transfusion and of persons identified as ‘at-risk’ of CJD (of any type) from other healthcare procedures. The GPs/clinicians of all persons identified as ‘at-risk’ for public health purposes are provided with: information; risk assessment updates; advice on public health precautions and advice on referral to specialist care. Procedures are being established to obtain enhanced surveillance data on these individuals, including: clinical status updates, date and cause of death, surplus tissue and blood specimens, and postmortem investigations.

Results:

Persons ‘at-risk’ of CJD have experienced a range of exposures. Estimated risks are uncertain and overlapping. Some individuals - recipients of vCJD implicated blood components - are considered to be at a clearly higher risk of infection: active follow-up is currently conducted for these individuals. In time, the enhanced surveillance of persons at increased risk of CJD will provide estimates of transmission risks and of the impact of iatrogenic exposures on mortality. Conclusion: Knowledge about iatrogenic transmission of CJD is being gained by the follow-up of individuals who have been identified as ‘at-risk’ of CJD in the UK. This enhanced surveillance may need to be sustained for many years.

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


Prions in Plasma of Patients with Sporadic Creutzfeldt-Jakob Disease Safar, J.G1,3, Geschwindm M.D2,3, Letessier, F1, Kuo, A1, Pomeroy, K1, Deering, C1, Serban, A1, Groth, D1, Miller, B.L2,3, DeArmond, S.J1,4, Prusiner, S.B1,3,5 1Institute for Neurodegenerative Diseases, 2Memory and Aging Center, Departments of 3Neurology, 4Pathology, and 5Biochemistry and Biophysics, University of California, San Francisco, California 94143

http://www.prion2007.com/pdf/Prion%20Friday.pdf


http://www.prion2007.com/pdf/Prion%20Thursday.pdf


http://www.prion2007.com/pdf/Prion%20Wednesday.pdf


October 3, 2007

October 2007 Update on Feed Enforcement Activities to Limit the Spread of BSE

To help prevent the establishment and amplification of Bovine Spongiform Encephalophathy (BSE) through feed in the United States, the Food and Drug Administration (FDA) implemented a final rule that prohibits the use of most mammalian protein in feeds for ruminant animals. This rule, Title 21 Part 589.2000 of the Code of Federal Regulations, here called the Ruminant Feed Ban, became effective on August 4, 1997.

The following is an update on FDA enforcement activities regarding the ruminant feed ban. FDA's Center for Veterinary Medicine (CVM) has assembled data from the inspections that have been conducted AND whose final inspection report has been recorded in the FDA's inspection database as of September 29, 2007. As of September 29, 2007, FDA had received over 57,000 inspection reports. The majority of these inspections (around 69%) were conducted by State feed safety officials, with the remainder conducted by FDA officials.

Inspections conducted by FDA or State investigators are classified to reflect the compliance status at the time of the inspection based upon the objectionable conditions documented. These inspection conclusions are reported as Official Action Indicated (OAI), Voluntary Action Indicated (VAI), or No Action Indicated (NAI).

An OAI inspection classification occurs when significant objectionable conditions or practices were found and regulatory sanctions are warranted in order to address the establishment's lack of compliance with the regulation. An example of an OAI inspection classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspections classified with OAI violations will be promptly re-inspected following the regulatory sanctions to determine whether adequate corrective actions have been implemented.

A VAI inspection classification occurs when objectionable conditions or practices were found that do not meet the threshold of regulatory significance, but do warrant advisory actions to inform the establishment of findings that should be voluntarily corrected. Inspections classified with VAI violations are more technical violations of the Ruminant Feed Ban. These include provisions such as minor recordkeeping lapses and conditions involving non-ruminant feeds.

An NAI inspection classification occurs when no objectionable conditions or practices were found during the inspection or the significance of the documented objectionable conditions found does not justify further actions. The results to date are reported here both by “segment of industry” and “in total”. NOTE – A single firm can operate as more than one firm type. As a result, the categories of the different industry segments are not mutually exclusive.

RENDERERS

These firms are the first to handle and process (i.e., render) animal proteins and to send these processed materials to feed mills and/or protein blenders for use as a feed ingredient.

Number of active firms whose initial inspection has been reported to FDA – 266

Number of active firms handling materials prohibited from use in ruminant feed – 155 (58% of those active firms inspected)

Of the 155 active firms handling prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

6 firms (3.9%) were classified as VAI

LICENSED FEED MILLS

FDA licenses these feed mills to produce medicated feed products. The license is required to manufacture and distribute feed using certain potent drug products, usually those requiring some pre-slaughter withdrawal time. This licensing has nothing to do with handling prohibited materials under the feed ban regulation. A medicated feed license from FDA is not required to handle materials prohibited under the Ruminant Feed Ban.

Number of active firms whose initial inspection has been reported to FDA – 1,071

Number of active firms handling materials prohibited from use in ruminant feed – 466 (44% of those active firms inspected)

Of the 466 active firms handling prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

8 firms (1.7%) were classified as VAI

FEED MILLS NOT LICENSED BY FDA

These feed mills are not licensed by the FDA to produce medicated feeds.

Number of active firms whose initial inspection has been reported to FDA – 5,163

Number of active firms handling materials prohibited from use in ruminant feed – 2,481 (48% of those active firms inspected)

Of the 2481 active firms handling prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

46 firms (1.9%) were classified as VAI

PROTEIN BLENDERS

These firms blend rendered animal protein for the purpose of producing quality feed ingredients that will be used by feed mills.

Number of active firms whose initial inspection has been reported to FDA – 392

Number of active firms handling materials prohibited from use in ruminant feed – 191 (49% of those active firms inspected)

Of the 191 active firms handling prohibited materials, their most recent inspection revealed that:

0 firm (0%) was classified as OAI

5 firms (2.6%) were classified as VAI

RENDERERS, FEED MILLS, AND PROTEIN BLENDERS MANUFACTURING WITH PROHIBITED MATERIAL

This category includes only those firms that actually use prohibited material to manufacture, process, or blend animal feed or feed ingredients.

Total number of active renderers, feed mills, and protein blenders whose initial inspection has been reported to FDA – 6,577

Number of active renderers, feed mills, and protein blenders processing with prohibited materials – 493 (7.5%)

Of the 493 active renderers, feed mills, and protein blenders processing with prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

24 firms (4.9%) were classified as VAI

OTHER FIRMS INSPECTED

Examples of such firms include ruminant feeders, on-farm mixers, pet food manufacturers, animal feed salvagers, distributors, retailers, and animal feed transporters.

Number of active firms whose initial inspection has been reported to FDA – 18,358

Number of active firms handling materials prohibited from use in ruminant feed – 5,911 (32% of those active firms inspected)

Of the 5911 active firms handling prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

177 firms (3.0%) were classified as VAI

TOTAL FIRMS

Note that a single firm can be reported under more than one firm category; therefore, the summation of the individual OAI/VAI firm categories will be more than the actual total number of OAI/VAI firms, as presented below.

Number of active firms whose initial inspection has been reported to FDA – 20,807

Number of active firms handling materials prohibited from use in ruminant feed – 6,602 (32% of those active firms inspected)

Of the 6602 active firms handling prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

190 firms (2.9%) were classified as VAI

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Issued by: FDA, Center for Veterinary Medicine, Communications Staff, HFV-12 7519 Standish Place, Rockville, MD 20855 Telephone: (240) 276-9300 FAX: (240) 276-9115 Internet Web Site: http://www.fda.gov/cvm

http://www.fda.gov/cvm/BSE1007.htm


What Do We Feed to Food-Production Animals? A Review of Animal Feed Ingredients and Their Potential Impacts on Human Health

Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly Walker1 1Johns Hopkins Center for a Livable Future, Bloomberg School of Public Health, Baltimore, Maryland, USA; 2Maryland Institute for Applied Environmental Health, College of Health and Human Performance, University of Maryland, College Park, Maryland, USA; 3Lisa Y. Lefferts Consulting, Nellysford, Virginia, USA

snip...

Table 1. Animal feed ingredients that are legally used in U.S. animal feeds

Animal

Rendered animal protein from Meat meal, meat meal tankage, meat and bone meal, poultry meal, animal the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell production animals and other meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal animals digest from dead, dying, diseased, or disabled animals including deer and elk Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and undried processed animal waste products

snip...

Sapkota et al. 668 VOLUME 115 NUMBER 5 May 2007 • Environmental Health Perspectives

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1867957&blobtype=pdf


10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

___________________________________

PRODUCT Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. Firm initiated recall is ongoing. REASON Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI

___________________________________

PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK- MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007 CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified. RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete. REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html


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.

PMID: 6997404

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to- human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.

snip...

BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa


It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s145d.pdf



6. It also appears to me that Mr Bradley’s answer (that it would take less than say 100
grams) was probably given with the benefit of hindsight; particularly if one
considers that later in the same answer Mr Bradley expresses his surprise that it
could take as little of 1 gram of brain to cause BSE by the oral route within the
same species. This information did not become available until the "attack rate"
experiment had been completed in 1995/96. This was a titration experiment
designed to ascertain the infective dose. A range of dosages was used to ensure
that the actual result was within both a lower and an upper limit within the study
and the designing scientists would not have expected all the dose levels to trigger
infection. The dose ranges chosen by the most informed scientists at that time
ranged from 1 gram to three times one hundred grams. It is clear that the designing
scientists must have also shared Mr Bradley’s surprise at the results because all the
dose levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml


Subject: Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route Date: September 29, 2007 at 12:50 pm PST

P04.27

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany

Background:

In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.

Aims:

The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.

Methods:

Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

Results:

In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.

Conclusions:

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.

The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).

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


Subject: Aspects of the Cerebellar Neuropathology in Nor98 Date: September 26, 2007 at 4:06 pm PST

P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway

Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes 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 histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. *** The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

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


From: "Terry S. Singeltary Sr." Sent: Tuesday, August 21, 2007 9:50 AM Subject: TWO MORE Nor98 atypical Scrapie cases detected in USA bringing total to 3 cases to date

Infected and Source Flocks

As of June 30, 2007, there were .....

snip...

One field case and one validation case were consistent with Nor-98 scrapie.

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps


IN the February 2007 Scrapie report it only mentions ;

''One case was consistent with Nor98 scrapie.''

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/


Subject: NOR-98 SCRAPIE UPDATE AUGUST 31, 2007 (RISES TO 5 DOCUMENTED CASES IN USA) Date: October 9, 2007 at 7:15 am PST

Greetings, seems the NOR-98 atypical scrapie cases are the rise in the USA. ...tss

INFECTED AND SOURCE FLOCKS

AS of August 31, 2007, there were 33 scrapie infected and source flocks with open statuses (Figure 3). Five new source flocks and one new infected flock were reported n August (Figure 4) with a total of 64 reported for FY 2007 (Figure 5).

snip...

IN FY 2007 TWO FIELD CASES, ONE VALIDATION CASE, AND TWO RSSS CASES WERE CONSISTENT WITH NOR-98 SCRAPIE. ...

(BRINGS A TOTAL OF 5 NOR-98 CASES DOCUMENTED IN 2007 IN USA. ...TSS)

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps


(please note flocks of origin were in WY, CO, AND CA. PERSONAL COMMUNCATIONS USDA, APHIS, VS ET AL. ...TSS)

NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=14553


An evaluation of scrapie surveillance in the United States

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=3427


FOIA REQUEST FOR ATYPICAL TSE INFORMATION ON VERMONT SHEEP

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=10451


Subject: FSIS NOTICE SAMPLE COLLECTION FROM CATTLE UNDER THE BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) ONGOING SURVEILLANCE PROGRAM From: "Terry S. Singeltary Sr." Reply-To: Sustainable Agriculture Network Discussion Group Date: Fri, 2 Feb 2007 17:32:58 -0600

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&P=720


ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007

Date: Mon, 24 Sep 2007 21:31:55 -0500

I suggest that you all read the data out about h-BASE and sporadic CJD, GSS, blood, and some of the other abstracts from the PRION2007. ...

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&F=&S=&P=19744


*** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF THIS !!! THE PRICE OF POKER INDEED GOES UP. ...TSS

USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779


see full text 143 pages ;

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


[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non- Ambulatory Disabled Cattle 03-025IFA 03-025IFA-2 9/13/2005

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf


THE SEVEN SCIENTIST REPORT ***

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf


PAUL BROWN M.D.

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf


9 December 2005 Division of Dockets Management (RFA-305)

SEROLOGICALS CORPORATION James J. Kramer, Ph.D. Vice President, Corporate Operations

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf


Embassy of Japan

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC240.htm


Dockets Entered on December 22, 2005 2005D-0330, Guidance for Industry and FDA Review Staff on Collection of Platelets by Automated ... EC 203, McDonald's Restaurants Corporation, Vol #:, 34 ...

http://www.fda.gov/ohrms/dockets/dailys/05/Dec05/122205/122205.htm


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

http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf


03-025IF 03-025IF-631 Linda A. Detwiler [PDF] Page 1. 03-025IF 03- 025IF-631 Linda A. Detwiler Page 2. Page 3. Page 4. Page 5. Page 6. Page 7. Page 8. Page 9. Page 10. Page 11. Page 12. http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-631.pdf


Transmissible Spongiform Encephalopathy UPDATE USA OCTOBER 2007

http://www.phxnews.com/fullstory.php?article=53128


CREUTZFELDT JAKOB DISEASE MAD COW BASE, CWD, SCRAPIE UPDATE OCT 2007

http://cjdmadcowbaseoct2007.blogspot.com/


Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518

flounder9@verizon.net

BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS

http://madcowtesting.blogspot.com/


MADCOW USDA the untold story

http://madcowusda.blogspot.com/


MADCOW USDA the untold story continued

https://www.blogger.com/comment.g?blogID=6472149427883113751&postID=4829467681293855400


USA NOR-98 SCRAPIE UPDATE AUGUST 31, 2007 RISES TO 5 DOCUMENTED CASES

http://nor-98.blogspot.com/


Government Accountability Project

https://www.blogger.com/comment.g?blogID=3995372399492420922&postID=295754279213239559


Transmissible Mink Encephalopathy TME

http://transmissible-mink-encephalopathy.blogspot.com/


TME hyper/drowsy, INTER-SPECIES TRANSMISSION CWD and strainproperties

https://www.blogger.com/comment.g?blogID=37955408&postID=116577315153980667


USA NVCJD BLOOD RECALLS ONLY ;

http://www.google.com/search?hl=en&q=CJD+BLOOD+RECALLS+TSS&btnG=Search


vCJD case study highlights blood transfusion risk

http://vcjdblood.blogspot.com/


CREUTZFELDT JAKOB DISEASE MAD COW BASE, CWD, SCRAPIE UPDATE OCT 2007

http://cjdmadcowbaseoct2007.blogspot.com/


TSEAC MEETINGS

http://tseac.blogspot.com/


MRSA

http://staphmrsa.blogspot.com/


ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007Date: Mon, 24 Sep 2007 21:31:55 -0500I suggest that you all read the data out about h-BASE and sporadic CJD, GSS,blood, and some of the other abstracts from the PRION2007. ...

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&F=&S=&P=19744


*** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF THIS !!! THE PRICE OFPOKER INDEED GOES UP. ...TSSUSA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling ittoday), please note that both the ALABAMA COW, AND THE TEXAS COW, both were''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 200711:52 PM. ...TSS

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779


From: "Terry S. Singeltary Sr."Subject: CWD UPDATE 88 AUGUST 31, 2007

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&P=450


PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increasein ''TYPE UNKNOWN''. ...TSS1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17inconclusive and 9 pending (1 from 2006, 8from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1from 2001, 1 from 2003, 4 from 2004, 3from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006,*** 26 from 2007)

http://www.cjdsurveillance.com/pdf/case-table.pdf


Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734.

http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535

There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection. He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf


doi:10.1016/S1473-3099(03)00715-1Copyright © 2003 Published by Elsevier Ltd.Newsdesk

Tracking spongiform encephalopathies in North America

Xavier Bosch

Available online 29 July 2003.

Volume 3, Issue 8, August 2003, Page 463“

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.”............................

http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/fulltext


http://download.thelancet.com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf


see history of cjd questionnaire

http://brain.hastypastry.net/forums/showthread.php?t=2408

if you will notice on the forms page on the cjd foundation site, there is not cjd questionnaire ??? strange...

http://www.cjdsurveillance.com/forms.html

vCJD questionnaire

http://www.bseinquiry.gov.uk/report/volume8/pdf/1stquestionnaire.pdf

USA WRITTEN CJD QUESTIONNAIRE ???

http://cjdquestionnaire.blogspot.com/

why is a cjd questionnaire not listed on the cjd foundation 'forms' site with the rest of their forms ??? i thought they had one now going out to all families of victims of a human TSE??? this is very important that a _written_ cjd questionnaire, asking extensive questions pertaining to any potential route and source of the TSE agent be submitted to every family of a victim of a human TSE. this is key to finding cause. so why is this still so difficult? are the families of CJD victims getting these written cjd questionnaires??? i hope so.... 2008

The statistical incidence of CJD cases in the United States has been revised to reflect that there is _one case per 9000 in adults age 55 and older_. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

http://www.cjdfoundation.org/fact.html

FDA FAILED US

http://fdafailedus.blogspot.com/

SCIENCE BUSHWHACKED

http://sciencebushwhacked.blogspot.com/

Sunday, July 20, 2008 Red Cross told to fix blood collection or face charges 15 years after warnings issued, few changes made to ensure safety

http://vcjdblood.blogspot.com/2008/07/red-cross-told-to-fix-blood-collection.html

Sent: Monday May 28, 2007 Subject: THE BIG LIE SPORADIC CJD AND MAD COW DISEASEs i.e. TSE

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0705&L=sanet-mg&T=0&P=25276


[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle

03-025IFA03-025IFA-2 Terry S. Singeltary

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf


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

http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf


BRITISH MEDICAL JOURNAL

BMJ

http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406


BMJ

http://www.bmj.com/cgi/eletters/320/7226/8/b#6117


CJD NEWS

http://disc.server.com/Indices/236650.html


CJD VOICE (voice for _all_ victims of human TSE)

http://members.aol.com/larmstr853/cjdvoice/cjdvoice.htm


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 Posted by Terry S. Singeltary Sr. at 12:07 PM 1 comments: Terry S. Singeltary Sr. said... 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, 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 year.......it is a big fat sponge...the agent continues to eat the brain ......you 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 action........it 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 chair........you 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 them.......like a buzzard to the bone...you 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.)

==========================================

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0612&L=sanet-mg&T=0&P=10326


http://brain.hastypastry.net/forums/archive/index.php/t-5581.html


see full text ;

http://disc.server.com/discussion.cgi?disc=7498;article=3473;title=CJD%20Voice%20Discussion%20Group


TSS