Saturday, July 17, 2010

TSE Road map 2 A Strategy paper on TSE, a road to no where

Brussels, 16.7.2010 COM(2010)384 final COMMUNICATION FROM THE COMMISSION TO THE EUROPEAN PARLIAMENT AND THE COUNCIL

The TSE Road map 2

A Strategy paper on Transmissible Spongiform Encephalopathies for 2010-2015 SEC(2010)899

1. INTRODUCTION

The first TSE1 Roadmap2, provided an outline of possible future changes to EU measures on TSEs in the short, medium and long-term while still making food safety and consumer protection the highest priority. The majority of short and medium term actions envisaged in the first TSE Roadmap have been achieved and the positive trend already observed in 2005 in the Bovine Spongiform Encephalopathy (BSE) epidemic has continued since then. At the same time, the impact of BSE on human health appears to be more limited than initially feared.

This Communication is complemented by a Commission Staff Working Document (CSWD) where Annexes referred to in the Communication can be found and which inter alia includes an overview of the achievements of the first TSE roadmap over the period 2005-2009.

The goal for the coming years is to continue the review of the measures while assuring a high level of food safety. Amendments to the TSE rules are and will continue to be taken following a stepwise approach supported by a solid scientific basis. In this respect, the scientific advice provided by the European Food Safety Authority (EFSA) should continue to play a crucial role to consider future policy options. It is also of paramount importance to continue research in those areas where information is lacking or gaps exist which do not allow firm decisions to be taken. The aim of this Communication is to outline future possible amendments allowing a review of the measures to align them with the situation where the EU is finally on the last pathway to eradicate BSE within its cattle population. However vigilance should be ensured in order to continue to monitor the situation in case of a potential reemergence of BSE or emergence of a new TSE agent in cattle population.

This review should be primarily driven by scientific advice and technical issues related to the control and enforcement of the new measures.

snip...

2.2.3. Possible gradual lifting of the feed ban

The starting point when revising the current feed ban provisions should be risk-based but at the same time should take into account the control tools in place to evaluate (i.e. the availability of a reliable test to identify the species of trace of MBM).

– Tolerance level for PAP in feed for farmed animals

In order to apply a risk-based approach in case prohibited PAP has been detected, a certain tolerance level may be established.

On December 2009, the Commission asked EFSA to provide an updated quantitative risk assessment on the risk linked to small amounts of processed animal proteins in feed. The EFSA opinion is expected by the end of 2010. Based on the EFSA conclusions, an introduction of a tolerance level with regard to a very small presence of PAP in feed may be proposed without jeopardising the current eradication measures. – Lifting feed ban provisions for non-ruminants (pigs, poultry, fishes) Currently, PAP forbidden for feeding purposes are used mainly to produce fertilizers, compost or carburant for cement works. However, PAP may be a source of proteins for non-ruminant farmed animals which need to be fed with high quality proteins.

Considering that the transmission risk of BSE from non ruminants to non-ruminants is very unlikely, a lifting of the ban on the use of PAP from non-ruminants in nonruminant feed could be considered, but without lifting the existing prohibition on intraspecies recycling (e.g. poultry MBM could only be fed to pigs and pig MBM to poultry). Moreover the reintroduction of PAP in non-ruminant feed may enable the EU to decrease the dependence on other sources of proteins.

Such a measure would however be acceptable only if validated analytical techniques to determine the species origin of PAP are available. In addition, considering the limitation

EN 8 EN

inherent in any control method, correct channelling of PAP from different species will be an important part of any review of the current feed ban provisions. The valorisation of PAP for feeding purposes will have to be compared to the investments needed to comply with the channelling requirements.

http://ec.europa.eu/food/food/biosafety/tse_bse/docs/roadmap_en.pdf



Sad isn't it. What's even more sad is the fact that the USA never did stop feeding cows to cows, and never ever really started to look for mad cows. They just played like they did with cattle that had already been deemed healthy, OR, used a test on thousands of cattle, a test least likely to find BSE (IHC only), OR just rendered any highly suspect stumbling and staggering mad cow, without any test at all, OR, let suspect BSE test samples sit on the shelf for months and months and months, as so the suspect BSE tissue sample is so old, proper testing could never be done, OR...... i could go on, but you get where i am going here. Fact is, this TSE Road map 2, is a road back in time. ...TSS



UK Food Standards Agency to be abolished - report By Rory Harrington, 12-Jul-2010

Related topics: Quality & Safety, Cleaning / Safety / Hygiene

The UK Food Standards Agency (FSA) is to be broken up with its food safety and nutritional roles handed over to separate government departments, according to reports.

The proposed abolition of the food watchdog would see its safety functions assigned to the Department for Environment, Food and Rural Affairs (Defra), while the Department of Health would lead on issues relating to public health nutrition and diet, said Reuters.

The Food and Drink Federation (FDF), a leading UK industry body, said it would wait for the announcement to be made before commenting but, in principle, believed in the need for a stand-alone food safety regulator.

Under review

The plan is thought to be part of swingeing cost-cutting measures tabled by the new coalition Government to reduce waste and bureaucracy. The Department of Health (DoH) today refused to confirm or deny the shake up ahead of announcing a string of new measures in its White Paper but FoodProductionDaily.com understands that the FSA will not be mentioned in the impending legislative proposals spearheaded by Minister Andrew Lansley.

“No decision has been taken over the Food Standards Agency (FSA),” said a DoH spokesperson. “All Arms Length Bodies will be subject to a review.”

Independent food safety regulator

If true, the proposal is likely to spark concern as the FSA was formed a decade ago after a number of major contamination crises such as BSE saw the collapse of public trust in the government’s ability to manage food safety. Questions were raised about a possible conflict of interest over a single department regulating both food producers and food processors. The formation of the FSA as a dedicated and independent watchdog was seen by many an effective way to address those anxieties.

The Food and Drink Federation, while stressing that it would wait to see the actual proposals, backed the need for a stand-alone food safety body.

“At the moment we are still unclear about what is actually happening with the FSA,” said a FDF spokesperson. “Andrew Lansley has always been pretty open about his intention to bring nutrition back into the Department of Health but we have always believed that there is a need for an independent well funded food safety regulator.”

http://www.foodproductiondaily.com/Quality-Safety/UK-Food-Standards-Agency-to-be-abolished-report


Don't shoot the watchdog - food industry needs a tight leash Post a commentBy Jane Byrne , 12-Jul-2010

Related topics: Quality & Safety

Watchdogs provide much needed protection in an uncertain world. So why is the UK government determined to kill off the Food Standards Agency?

Safer food, healthier eating for all and informed choices, the three priorities of the FSA, will inevitably be compromised by UK health secretary Andrew Lansley’s decision to switch to a business funded model for the drive against child obesity - Change4Life - coupled with his pre-election pledge to carve up the FSA now looking set to see the light of day.

The duties of the FSA in relation to safety and hygiene in the food chain will be subsumed by the Department for Environment, Food and Rural Affairs (Defra) and its nutrition functions will transfer to the Department of Health, according to a report on Reuters.

These cost-cutting measures are using a recipe not formulated with the state of public health in mind but using instead a quick fix solution for a cash-strapped government.

The Conservative-Liberal Democrat coalition, in power since May, is looking for dramatic budget cuts to reduce the £156bn deficit but can a price be put on food safety and the long term health impact of food lower in saturated fats and salt?

In 1997 public confidence in UK food had been torn to shreds by BSE. The only way Labour could reconstruct it was by disentangling business interests from policy-making and making dealings transparent.

Hello FSA and a renewed sense of food safety assurance 10 years later.

And the food watchdog’s approach to raising consumer awareness about healthier diets, while engaging with the food industry on voluntary reformulation for reduced salt, sugar and saturated fat, has been pioneering and a model adopted by many other countries.

Now Lansley wants food and drink makers to bankroll the anti-obesity drive Change4Life in return for no regulation. How will the minister ensure that such an approach guarantees that industry only funds the campaign but does not control it?

And really, however much reformulation work has been done to date by food companies, would they really keep that up if the pressure from the FSA was off?

Surely a switch to positive images of people exercising on breakfast cereals and fizzy drinks packaging would be a less burdensome option than further reductions in salt and sugar?

Tam Fry, honorary chairman of the anti-obesity campaign the Child Growth Foundation, said that Change4Life is the sort of campaign that needs a lot of funding and a long-term view.

“If we are trying to change behaviours, that does not happen overnight, only after years and years of constant reminders."

With high rates of weight gain and lack of sports activity by children, rising National Health Service (NHS) bills for diabetes, heart disease and cancer, the risks are too high to leave the promotion of a healthy lifestyle to food and drinks manufacturers alone.

Change4Life needs investment by government - it might be costly, but it could cut the bills of the UK health service in the long term.

As regards the proposed splitting up of the FSA – we only have to look to the number of food safety scares in the US to see the consequences of its fragmented food safety approach.

So instead of putting the food watchdog to sleep, shouldn’t the UK government instead give it more teeth?

http://www.foodproductiondaily.com/Quality-Safety/Don-t-shoot-the-watchdog-food-industry-needs-a-tight-leash


Former EFSA chief calls on UK to keep FSA By Rory Harrington, 13-Jul-2010

Related topics: Quality & Safety, Cleaning / Safety / Hygiene

Abolishing the UK Food Standards Agency (FSA) would be a backward step that could sacrifice the body’s independent science-based approach and push food policy formation back into the political arena, former EFSA chairman Professor Patrick Wall told FoodProductionDaily.com.

Leading food safety expert Prof Wall was responding to reports of UK Government plans to dismantle the FSA and hand over its roles to separate departments. He said such a move could be a “huge mistake” and would be a blow for both consumers and producers.

While acknowledging reform of the agency was needed, he said no government department could hope to match the FSA’s standing and reputation for transparency.

“A reform of the FSA is probably timely but its complete abolition would be a retrograde step,” he said. “Its brand name is well recognised on the global stage and stands for transparency, credibility, integrity and sound science - adjectives that will never describe a government department.”

The associate professor of public health at University College Dublin mounted a robust defence of the need for the independent and apolitical food safety body set up in 2000. He said the agency was formed after a string of crises had undermined public confidence in the safety of the UK’s food supply.

The body is also one EU agency taking a trailblazing approach in pursuing reform of safety along food supply chain and it would be “a tragedy if this momentum were lost” as a result of the UK Government shake up, he said.

Conflict of interest

Creation of the FSA had been “a courageous and radical approach where a non ministerial department was created that could make, and implement policy and reassure consumers that their interests were paramount”, said Prof Wall. He added that the need to separate the functions of government that support the agriculture and food sectors from those that control it had been well-recognised across the European Union and pointed out the concerns many had harboured over the former UK ministry’s conflict of interests in performing both roles.

“The former UK Ministry of Agriculture, Fisheries and Food was perceived to be suffering from CJD - ‘conflicting job description’ - trying to protect the industry and the public’s health at the same time and succeeded in doing neither well”, he said.

Political agenda

He pointed out that the Department for Environment, Food and Rural Affairs (Defra) was dedicated to developing the agrifood sector and questioned whether it was “wise” to also give it responsibility for “reassuring consumers that their interests are being put before that of industry”.

Before the FSA’s inception, policy and priority setting for food safety and nutrition was often based on the amount of media coverage rather than risk to public health, said Prof Wall. The agency, with its transparent science-based decisions, had credibility with consumers. It proved to be the model on which many other European agencies was modelled and he cautioned against its eradication.

“The FSA has one of the best scientific advisory structures in the world and to dismantle this and go back to a politically set agenda may be a huge mistake and both the agrifood sector and consumers could be losers”, he said.

FSA reform

However, Prof Wall said the agency could need to be reformed as the UK “may have gone too far in conveying the power to make policy and implement it with the one body and creating a government department with no Minister”.

The UK Government has refused to confirm or deny plans to break up the FSA but said it was “under review”.

http://www.foodproductiondaily.com/Quality-Safety/Former-EFSA-chief-calls-on-UK-to-keep-FSA


IFST: Dismantling FSA would be "huge loss" to industry By Elaine Watson, 14-Jul-2010

Related topics: Legislation

Press reports suggesting that breaking up the Food Standards Agency (FSA) would constitute a ‘victory’ for the food industry are misleading and “very annoying”, according to the boss of the Institute of Food Science & Technology (IFST).

Speaking to FoodManufacture.co.uk as speculation over the future of the FSA reached fever pitch this week, IFST chief executive Jon Poole (pictured) said: “The suggestion that the food industry had ‘won a battle’ by pressuring the government to abolish or break up the FSA is really quite annoying.

“In reality, the demise of the FSA would be regarded by many people in the food industry as a huge loss. And in my view, the position of relative independence it has now is worth preserving. Very few in the sector will see the break up of the FSA as a positive step.”

He added: “It might have appeared a bit nanny state in terms of some of the work it was doing on nutrition, but in fact it has been acting as the conscience of the public and of the food industry itself.”

Industry is not at war with the FSA

The IFST (an independent professional body that accredits scientists and technologists in the food sector) had always enjoyed a “constructive and positive relationship” with the FSA, he added. “The adversarial style of relationship suggested in these press reports is neither accurate nor particularly helpful.”

While it had attracted the most column inches for its work on ‘traffic light’ labelling and salt reduction, the FSA had also “provided coherent strategy and direction around key food issues such as reductions in the levels of saturated fat and salt, reductions in campylobacter in chicken as well as regulating food business operators”, he added.

“These are all still very live issues and the functions of the FSA, in whatever form, will continue to be needed in the future."

Abolishing FSA is bad news for business

Eversheds partner David Young agreed that the demise of the FSA would not be good news for the food industry.

“The FSA has not been a foe of business by any means, affording manufacturers and other industry groups opportunities for access to its staff and expertise, input into consultations, involvement in its committees and the weight of its status when, from time to time, it has endorsed suggestions emanating from the industry.”

Former European Food safety Authority chairman Professor Patrick Wall also waded into the debate this week, telling our sister title FoodProductionDaily.com that breaking up the FSA would be a "huge mistake", while former FSA chairman Lord Krebs also warned that public trust in food safety would be put at risk were the FSA dismantled during a debate on nanotechnology last night.

He said: "I hope that the Minister will take this opportunity to confirm that newspaper reports of the FSA’s imminent demise are exaggerated."

No decision taken

Earl Howe, parliamentary under secretary of state in the Department of Health, was then forced to reiterate that no decision on the FSA had yet been taken, adding: "The noble Lord is assuming that the FSA is going to disappear. I have seen those reports but do not recognise the stories at all.

"No decisions have been taken about the future of various functions within the Food Standards Agency, but we are clear that there has to be a role for a body setting standards objectively in the way that he has described."

http://www.foodqualitynews.com/Legislation/IFST-Dismantling-FSA-would-be-huge-loss-to-industry




To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2




I ask Professor Kong ;

Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment

''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''

Professor Kong reply ;

.....snip

''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete.

Thanks for your interest.''

Best regards,

Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA

END...TSS

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.

http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf




Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009

http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html




atypical BSE MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN


18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.

snip...

64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.

snip...

http://www.seac.gov.uk/minutes/95.pdf


3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.***

6:30 Close of Day One

http://www.healthtech.com/2007/tse/day1.asp


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


2008 - 2010

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


CJD SURVEILLANCE TEXAS

http://cjdtexas.blogspot.com/2007/12/creutzfeldt-jakob-disease-surveillance.html


Friday, November 30, 2007

CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION

http://cjdquestionnaire.blogspot.com/


Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (TRANSCRIPT)

http://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/UCM171810.pdf


Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)

http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html


Saturday, June 13, 2009

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

http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html


Friday, February 05, 2010

New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review

http://vcjd.blogspot.com/2010/02/new-variant-creutzfelt-jakob-disease.html


Saturday, January 2, 2010

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

http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html


my comments to PLosone here ;


http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd



Saturday, June 19, 2010

U.S. DENIED UPGRADED BSE STATUS FROM OIE

see full text and reasons why here ;

http://usdameatexport.blogspot.com/2010/06/us-denied-upgraded-bse-status-from-oie.html


Saturday, June 12, 2010

PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse


http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html


CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER


>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<< http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8




>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<< http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo-cjd-victim-she-died.html



CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER


http://cjdtexas.blogspot.com/2010/03/cjd-texas-38-year-old-female-worked.html



Archive Number 20100405.1091 Published Date 05-APR-2010 Subject PRO/AH/EDR> Prion disease update 1010 (04)

snip...

[Terry S. Singeltary Sr. has added the following comment:

"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.

The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"


http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101


Tuesday, June 1, 2010

USA cases of dpCJD rising with 24 cases so far in 2010

http://cjdtexas.blogspot.com/2010/06/usa-cases-of-dpcjd-rising-with-24-cases.html


14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)

18.173 page 189

Experimental Challenge of Cattle with H-type and L-type Atypical BSE

A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada

Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.

Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.

Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.


http://www.isid.org/14th_icid/


http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf


http://www.isid.org/publications/ICID_Archive.shtml


14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America

update October 2009

T. Singeltary

Bacliff, TX, USA

Background:

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

Methods:

12 years independent research of available data

Results:

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 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

Conclusion:

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, 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.

http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf


Wednesday, March 31, 2010

Atypical BSE in Cattle

http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html



P2-110

TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY TO MICROCEBUS MURINUS, A NON-HUMAN PRIMATE. DEVELOPMENT OF CLINICAL SYMPTOMS AND TISSUE DISTRIBUTION OF PRPRES

Nadine Mestre-Frances1, Anne-Gaelle Biacabe2, Sylvie Rouland1, Thierry Baron2, Jean-Michel Verdier1, 1INSERM U710, Montpellier, France; 2AFSSA, Lyon, France. Contact e-mail: nfrances@univmontp2. fr

Background: Atypical BSE cases have been observed in Europe, Japan and North America. They differ in their PrPres profiles from those found in classical BSE. These atypical cases fall into 2 types, depending on the molecular mass of the unglycosylated PrPres band observed by Western blot: the L-type (lower molecular mass than the typical BSE cases) and H-type (higher molecular mass than the typical BSE cases).

Methods: Height animals (4 males and 4 females) were intracerebrally inoculated with 50 l of a 10% brain homogenates of atypical (L and H-type) French BSE cases.

Results: Only one of the four lemurs challenge with H-type BSE died without clinical signs after 19 months post inoculation (mpi), the 4 animals inoculated with L-type BSE died at 19 mpi (2 males) and 22 mpi (2 females). Three months before their sacrifice, they developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms get worse according to the disease progression, until severe ataxia. The brain tissue were biochemically and immunocytochemically investigated for PrPres. For the H-types, spongiform changes without PrPres accumulation were observed in the brainstem. Western blot analysis confirmed that no PrPres was detected into the brain. For the L-types, severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem, whereas into the cortex the spongiosis was evidenced, but the vacuolisation was weaker. Strong deposits of PrPres was detected by western blot, PET-blot and immunocytochemistry in the CNS: dense accumulation was observed into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques. Western blot analysis confirmed the presence of protease-resistant prion protein.

Conclusions: L-type infected lemurs showed survival times considerably shorter than for classical BSE strain, indicating that the disease is caused by a very virulent distinct prion strain.


http://download.journals.elsevierhealth.com/pdfs/journals/1552-5260/PIIS1552526008013447.pdf




>>> Conclusions: L-type infected lemurs showed survival times considerably shorter than for classical BSE strain, indicating that the disease is caused by a very virulent distinct prion strain. >>>


seems the survival time was the same for the h-type BSE and the l-type BSE i.e. 19 months post inoculation (mpi), interesting. ...TSS




Thursday, July 15, 2010

Effect of autolysis on the specificity of bovine spongiform encephalopathy rapid tests

http://madcowtesting.blogspot.com/2010/07/effect-of-autolysis-on-specificity-of.html


Thursday, June 24, 2010

Accumulation of L-type Bovine Prions in Peripheral Nerve Tissues

Volume 16, Number 7–July 2010

http://bse-atypical.blogspot.com/2010/06/accumulation-of-l-type-bovine-prions-in.html


Sunday, April 18, 2010

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html


Sunday, March 28, 2010

Nor-98 atypical Scrapie, atypical BSE, spontaneous TSE, trade policy, sound science ?

http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html


Saturday, June 5, 2010

Research Project: Transmissible Spongiform Encephalopathies: Identification of atypical scrapie in Canadian sheep

http://nor-98.blogspot.com/2010/06/research-project-transmissible.html


Monday, June 14, 2010

A molecular switch controls interspecies prion disease transmission in mice

http://chronic-wasting-disease.blogspot.com/2010/06/molecular-switch-controls-interspecies.html


Friday, May 14, 2010

Prion Strain Mutation Determined by Prion Protein Conformational Compatibility and Primary Structure

Published Online May 13, 2010 Science DOI: 10.1126/science.1187107 Science Express Index

http://chronic-wasting-disease.blogspot.com/2010/05/prion-strain-mutation-determined-by.html


http://chronic-wasting-disease.blogspot.com/


THE August 4, 1997 was a voluntary and partial feed ban.

IT was nothing more than ink on paper. ...TSS


10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED 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/Safety/Recalls/EnforcementReports/2007/ucm120446.htm



Tuesday, March 2, 2010

Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA

http://madcowfeed.blogspot.com/2010/03/animal-proteins-prohibited-in-ruminant.html


Monday, March 1, 2010

ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010

http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html


Sunday, January 17, 2010

BSE USA feed inspection violations 01/01/2009 to 01/17/2010 FDA BSE/Ruminant Feed Inspections Firms Inventory Report

http://madcowfeed.blogspot.com/2010/01/bse-usa-feed-inspection-violations.html


Friday, January 15, 2010

New York Firm Recalls Beef Carcass That Contains Prohibited Materials (BSE)

http://bse-atypical.blogspot.com/2010/01/new-york-firm-recalls-beef-carcass-that.html


Thursday, November 12, 2009

BSE FEED RECALL Misbranding of product by partial label removal to hide original source of materials 2009

http://madcowfeed.blogspot.com/2009/11/bse-feed-recall-misbranding-of-product.html


Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009

http://madcowfeed.blogspot.com/2009/09/foia-request-on-feed-recall-product.html


Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009

http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html



C O N F I R M E D


----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Thursday, November 05, 2009 9:25 PM
Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009

http://madcowfeed.blogspot.com/2009/11/re-foia-request-on-feed-recall-product.html


Thursday, November 12, 2009

BSE FEED RECALL Misbranding of product by partial label removal to hide original source of materials 2009

http://madcowfeed.blogspot.com/2009/11/bse-feed-recall-misbranding-of-product.html


CVM Annual Report Fiscal Year 2008: October 1, 2007-September 30, 2008

PUTTING LIPSTICK ON A PIG AND TAKING HER TO A DANCE...TSS

BSE Feed Rule Enforcement: A Decade of Success OFF TO A FAST START

http://madcowfeed.blogspot.com/2008/06/texas-firm-recalls-cattle-heads-that.html


Thursday, April 9, 2009

Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed

http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html


Thursday, March 19, 2009

MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL

http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html


Wednesday, January 13, 2010

Meat and bone meal back into feed 12 Jan 2010

http://madcowfeed.blogspot.com/2010/01/meat-and-bone-meal-back-into-feed-12.html


FDA et al thinks as much as 5.5 grams of SRM is just fine for a heifer weighing about 600 lbs ;

''FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.''

http://www.fda.gov/ICECI/EnforcementActions/EnforcementStory/EnforcementStoryArchive/ucm107472.htm



PRION 2009 CONGRESS BOOK OF ABSTRACTS

O.4.3

Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission

Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany

Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).

Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.

Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.

Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.

Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf


Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.

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


WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.

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 Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

http://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf


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

http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.

http://www.oie.int/boutique/extrait/06heim937950.pdf


IN A NUT SHELL ;

(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,

http://www.oie.int/eng/Session2007/RF2006.pdf


Monday, November 23, 2009

BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.

http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html


Docket APHIS-2006-0026 Docket Title Bovine Spongiform Encephalopathy; Animal Identification and Importation of Commodities Docket Type Rulemaking Document APHIS-2006-0026-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions, Identification of Ruminants and Processing and Importation of Commodities Public Submission APHIS-2006-0026-0012 Public Submission Title Comment from Terry S Singletary

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801e47e1


Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028 Public Submission Title Comment from Terry S Singletary

Comment 2006-2007 USA AND OIE POISONING GLOBE WITH BSE MRR POLICY

THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted products from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone. These are the facts as I have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species.

MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???

go figure. ...

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8151


Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028.1 Public Submission Title Attachment to Singletary comment

January 28, 2007

Greetings APHIS,

I would kindly like to submit the following to ;

BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f8152&disposition=attachment&contentType=msw8


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.

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf



WHO WILL WATCH THE CHILDREN FOR CJD OVER THE NEXT 5 + DECADES ???

Do you actually believe that the USDA et al jumped in on the law suit against Westland/Hallmark, at the time the largest beef recall in USA history, just because a few animals were abused on a video, or to cover their ass, for letting our children, from school district to school district, from state to state, be fed dead stock downer cows.


>>> In the papers, the government alleges the meatpacking plant slaughtered and processed downer cows for nearly four years — from January 2004 to September 2007 — at the average rate of one every six weeks... <<<


http://downercattle.blogspot.com/2009/09/suit-meatpacker-used-downer-cows-for-4.html


Do you actually believe all these schools recalled this meat because of a few cattle being abused, see list ;


FNS All Regions Affected School Food Authorities By State United States Department of Agriculture Food and Nutrition Service National School Lunch Program March 24, 2008 School Food Authorities Affected by Hallmark/Westland Meat Packing Co. Beef Recall February 2006 - February 2008


http://www.fns.usda.gov/fns/safety/Hallmark-Westland_byState.pdf


http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf#xml=http://65.216.150.153/texis/search/pdfhi.txt?query=Hallmark/Westland+Meat+Packing+Co.+Beef+Recall&pr=FNS&prox=page&rorder=500&rprox=500&rdfreq=500&rwfreq=500&rlead=500&rdepth=0&sufs=0&order=r&cq=&id=4bc8d6e114



IF url does not work above, go to this link to find out if any of your children and their school were part of this recall ;

go to this site ;


http://www.fns.usda.gov/fns/


left hand corner search ; Hallmark/Westland Meat Packing Co. Beef Recall your should get this ;


http://65.216.150.153/texis/search?pr=FNS


1 through 1 of 1 matching documents, best matches first. sort by date 1: Hallmark - Westland SFA Reporting by State - 3-24-2008.xls Lunch Program March 24, 2008 School Food Authorities Affected by Hallmark/Westland Meat Packing Co. Beef Recall February 2006 - February 2008 The U.S. Department of Agriculture ...


http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf#xml=http://65.216.150.153/texis/search/pdfhi.txt?query=Hallmark/Westland+Meat+Packing+Co.+Beef+Recall&pr=FNS&prox=page&rorder=500&rprox=500&rdfreq=500&rwfreq=500&rlead=500&rdepth=0&sufs=0&order=r&cq=&id=4bc8d6e114


PLEASE SEE ALSO ;



Members of The HSUS are also concerned about the meat products provided to their children through the National School Lunch Program. More than 31 million school children receive lunches through the program each school day. To assist states in providing healthful, low-cost or free meals, USDA provides states with various commodities including ground beef. As evidenced by the HallmarkNVestland investigation and recall, the potential for downed animals to make their way into the National School Lunch Program is neither speculative nor hypothetical.



http://biotech.law.lsu.edu/cases/FDA/hsus-v-schafer-usda-complaint.pdf



SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE


http://downercattle.blogspot.com/2009/05/who-will-watch-children.html


http://downercattle.blogspot.com/



PLEASE NOTE *


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


snip...


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


http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf



THEY KNEW 2 DECADES AGO the damn BSE mad cow testing were not finding cases ;

BSE-NON-CONFIRMATION OF DISEASE

3. A question posed by Mr Whaley (para 2) is that classical lesions of BSE may not occur in all cases. Supposing we had a strain variant that produced it's lesions in the cerebrum these would not be detected by our current method. I think this would be unlikely but not impossible - another reason why at least a proportion of complete brains (or blocks) should be retained during the epidemic so if the problem Mr Whaley indicates escalates, it can be investigated.

snip...

5. IF you had the information what benefit would there be ? what would you do with it ?

CONCLUSION

I do not recommend any action. The situation should be accepted. I do not think the VIS can do more at present. The situation should be kept under review particularly if there is an escalation in numbers in this category.

R BRADLEY

15 MAY 1990

90/5.15/3.2

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1990/05/15003001.pdf


http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1990/05/15003001.pdf


Tuesday, November 17, 2009

SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1

http://bse-atypical.blogspot.com/2009/11/seac-new-results-on-idiopathic.html


NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009

http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html


FOR ANYONE THAT DID NOT SEE THE COMMENT ABOVE, HERE IT IS AGAIN ;

2009 ''ALL OF THE 15 CATTLE TESTED SHOWED THAT THE BRAINS HAD ADNORMALLY ACCUMULATED PrP''

AND THE USDA ET AL KNEW IT TOO ;

""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."

THIS WAS DONE FOR A REASON!

THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS

USDA 2003

We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip.............

Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.

Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip...

FULL TEXT;

Completely Edited Version PRION ROUNDTABLE

Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado

END...TSS

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

http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf


Sunday, May 18, 2008

BSE, CJD, and Baby foods (the great debate 1999 to 2005)

http://bseinquiry.blogspot.com/2008/05/bse-cjd-and-baby-foods-great-debate.html


Sunday, May 18, 2008

MAD COW DISEASE BSE CJD CHILDREN VACCINES

http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html


Monday, May 19, 2008

SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS


http://bseinquiry.blogspot.com/2008/05/sporadic-cjd-in-farmers-farmers-wives.html



Sunday, February 14, 2010

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

http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html


PLEASE SEE FULL TEXT 98 PAGES HERE ;

[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


Response to Public Comments on the Harvard Risk Assessment of Bovine Spongiform Encephalopathy

Update, October 31, 2005 INTRODUCTION 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: http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp). 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:

http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf


another question, just how long have these atypical BSE TSEs been around in the bovine ???

let's look at another case of atypical BSE in Germany way back in 1992 ;

Subject: atypical BSE reported in 1992 and conviently slaughterd and incinerated and then swept under rug for about 12 years Date: April 26, 2007 at 1:08 pm PST 1992

NEW BRAIN DISORDER

3. WHAT ABOUT REPORTS OF NEW FORM OF BSE?

THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN THE HISTOPATHOLOGY AND INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS NOT BSE.

4. IS THIS NEW BRAIN DISORDER A THREAT?

WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE, AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. .......

http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/26001001.pdf


2. The Collinge/Will dispute appears to rumble on. Dr. Collinge had told Dr. Tyrrell that Dr. Will's response to his criticism about sharing material had been ''quite unacceptable'' (in spite of it's apparently conciliatory tone). Apparently Professor Allen was now going to try and arrange a meeting to resolve the dispute. No action here for MAFF, although Mr. Murray may be interested.

3. Dr. Tyrrell regretted that the Committee had not seen the article on BBD. However he felt that for the time being NO specific action was called for. The most important need was to consider the possibility that the condition might be transmissible. As we have discussed, I suggested that we might circulate a paper to the members of the committee giving our appreciation of this condition (and perhaps of other non-BSE neurological conditions that had been identified in negative cases) and of any necessary follow up action. IF any Committee member felt strongly about this, or if the issue CAME TO A HEAD, we would call an interim meeting. He was happy with this approach. I would be grateful if Mr. Maslin could, in discussion with CVL and veterinary colleagues draft such a note, which will presumably very largely follow what Mr. Bradley's briefing paper has already said, taking account of DOH comments, We can then clear a final version with DOH before circulating it to Committee members.

http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/29005001.pdf


IN CONFIDENCE

This is a highly competitive field and it really will be a pity if we allow many of the key findings to be published by overseas groups while we are unable to pursue our research findings because of this disagreement, which I hope we can make every effort to solve.

http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/26002001.pdf


COLLINGE THREATENS TO GO TO MEDIA


http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf


Wednesday, August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ? August 20, 2008

http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html


Thursday, July 08, 2010

Nosocomial transmission of sporadic Creutzfeldt-Jakob disease: results from a risk-based assessment of surgical interventions Public release date: 8-Jul-2010

http://creutzfeldt-jakob-disease.blogspot.com/2010/07/nosocomial-transmission-of-sporadic.html



Tuesday, July 13, 2010 CJD U.K. PARLIAMENT 12 July 2010 : Column 472W

The United Kingdom Parliament

http://vcjdtransfusion.blogspot.com/2010/07/cjd-uk-parliament-12-july-2010-column.html



re-TSE Road map 2 A Strategy paper on Transmissible Spongiform Encephalopathies for 2010-2015 SEC(2010)899


WE have lost the battle. I saw the writing on the wall when the OIE and the USDA et al changed the game from BSE GBR to BSE MRR, and when SEAC et al refused to take sporadic CJD seriously, and completely whitewashed BSE again with the IBNC junk science. It was all about money. Not enough _documented_ body bags, to date. Hell, how in the world can you document something, when nobody wants to document it. All one has to do is look at the terribly flawwed CJD and or BSE TSE surveillance progams, especially here in the USA, or the lack of. Check mate. Industry et al wins. Junk political science prevails with human and animal TSE, and this dog and pony show will begin to import and export all strains of TSE globally again, thanks to the OIE, the USDA, the BSE MRR policy, and this TSE Road map 2, a road to no where, but bact were we were in 1985. TSE Road map 2 A Strategy paper on TSE, a road to no where but back in time, except this time, up front, we know some strains are more virulent, many times more virulent. so let's relax the rules $$$

a road to no where...

Thursday, July 08, 2010

GLOBAL CLUSTERS OF CREUTZFELDT JAKOB DISEASE - A REVIEW 2010

snip...

IN CLOSING, I wish to say that if anyone still thinks that 85% to 90% of all sporadic CJD is a spontaneous happening without any route and source of the TSE agent, just a happen stance of bad luck, as some officials still claim today, as with every hospital that has a CJD exposure accident will tell you, if anyone still believes this, they should then go and resign from whatever scientific and or doctors field you practice in, because YOU are then partially responsible for the continued spread of this horrible disease around the Globe. For Pete's sake, if clusters happen with animal TSE, then why not humans? IF all these TSE transmit to many different animal species, both in the field and in the lab, what make's it so hard to believe that it will not transmit to humans? IF all these TSE in all these many different species, with all these many different strains now appearing, both typical and atypical, with over 20 strains in just typical scrapie alone, nor-98 atypical scrapie, with BSE freely transmitting to sheep as well, now 4 BSE strains in cattle i.e. c-BSE, l-BSE, h-BSE, and IBNC (prion gods will have to admit this is a prion TSE disease sooner or later), now 2 strains of CWD documented i.e. CWD-1 and CWD-2, and the TME with the drowsy TME strain and the hyper TME strain, if all this has been fed to humans and to livestock producing animals for human and animal consumption, then what would human TSE there from look like, either from consumption, or 2nd, 3rd, 4th passage via friendly fire i.e. via surgical, dental, blood, medical arenas, from humans exposed by consumption ? NOT to forget all the animal medical by-products there from too? BUT yet, officials will still try and have us believe that 85% to 95% of all human Transmissible Spongiform Encephalopathy TSE i.e. sporadic CJD, is a single strain, that just happens spontaneously, with no route and source from anything. P L E A S E, This is not rocket science. It's 2010, and the UKBSEnvCJD only theory should be put to rest once and for all. Iatrogenic CJD is spreading as we speak, there are many strains, they are becoming more virulent, and they came from some route and some source, and that could be many. North America is home to the most strains of documented natural field TSE in animals. These animals have been fed to both humans and animals for human consumption. The consumer there from are a source of TSE to the medical and surgical arena, and clusters there from are real, they are happening and there is a route and source. CJD and all human TSE prion disease must be made mandatory reportable, with NO age limits, with a CJD Questionnaire asking real questions pertaining to potential routes and sources going to all families of victims of this horrible disease. This must be done Nationally and Internationally immediately. We have floundered too long. ...

tarball, aka flounder, alias TSS, and for those that remember, madcowdeadmommadson

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

PLEASE SEE FULL TEXT WITH SOURCE DATA ON DIFFERENT CJD CLUSTERS AROUND THE GLOBE (i am sure i missed some) ;

Thursday, July 08, 2010

GLOBAL CLUSTERS OF CREUTZFELDT JAKOB DISEASE - A REVIEW 2010


http://creutzfeldt-jakob-disease.blogspot.com/2010/07/global-clusters-of-creutzfeldt-jakob.html



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



*** UPDATE ON TSE roadmap 2, a road to no where Sunday July 18, 2010 ***



IN reply to ;


Saturday, July 17, 2010

TSE Road map 2 A Strategy paper on TSE, a road to no where

Brussels, 16.7.2010 COM(2010)384 final COMMUNICATION FROM THE COMMISSION TO THE EUROPEAN PARLIAMENT AND THE COUNCIL

http://transmissiblespongiformencephalopathy.blogspot.com/2010/07/tse-road-map-2-strategy-paper-on-tse.html


Confucius is confused again. IF BSE was spontaneous, just happens from nothing occasionally, from a funked out twisted protein, that just happens to spontaneously change shapes on it's own, as most officials have had us believe over the years, decades. THEN how is BSE almost eradicated ??? hmm?

WHAT about atypical BSE's ?

WHAT about IBNC BSE ?

SRM's there from all of the above ?

WHAT about SRM from pigs, poultry, fish, AND the potential for passing the TSE agent surviving the digestinal track to expose further in feed ?

The potential for transmissible spongiform encephalopathies in non-ruminant livestock and fish

D. Matthews (1) & B.C. Cooke (2) (1) Transmissible Spongiform Encephalopathy [TSE) Programme Manager, Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone. Surrey KT15 3NB. United Kingdom (2) 1 Jenkins Orchard, Wick St Lawrence. Weston Super Mare. North Somerset, BS22 7YP. United Kingdom

Summary

Pigs and poultry in the United Kingdom have undeniably been exposed to the bovine spongiform encephalopathy (BSE) agent. They consumed the same ruminant protein that gave rise to the BSE epidemic in cattle, but there has been no evidence of an epidemic in these species. Experimental investigations have shown pigs to be susceptible to infection by multiple parenteral challenge, but resistant to oral exposure with BSE-infected cattle brain. Current but incomplete evidence suggests that they are also resistant to oral challenge with sheep scrapie. Studies in domestic chickens indicate that they are resistant to both parenteral and oral challenge. Unfortunately, no published data exists on the susceptibility of fish to infection. Incidental findings in the brains of unexposed pigs are described that could otherwise give rise to concerns about the presence of a transmissible spongiform encephalopathy in pig populations around the world.

Keywords

Chicken - Fish - Meat-and-bone meal - Pig - Poultry - Prion - Prion protein ­Transmissible spongiform encephalopathy.

Introduction

The recognition of bovine spongiform encephalopathy (BSE) in domestic cattle in the United Kingdom (UK) in 1986 inevitably led to concerns about the potential risk to non-ruminant livestock (49). Although the initial focus was on the identification of the causal agent of BSE and confirmation that the disease was transmissible (20), research rapidly investigated the likelihood that pigs and poultry might also be susceptible to infection. lnitial epidemiological investigations into the source of BSE identified the likely vehicle to be the consumption by cattle of rendered animal protein of ruminant origin (51). With time, the decline of the epidemic following the implementation of measures to remove ruminant protein from cattle feed has confirmed that hypothesis. This is distinct from the debate about whether the actual origin of the agent was ovine or bovine. While there has been speculation about whether BSE arose spontaneously in bovines, rather than from transmission of sheep scrapie to cattle, the ban dealt with the vehicle of transmission, irrespective of origin.

http://www.oie.int/boutique/extrait/18matthews.pdf


Wednesday, April 02, 2008 In vivo prion protein intestinal uptake in fish

1: APMIS. 2008 Mar;116(3):173-80.

In vivo prion protein intestinal uptake in fish.

Dalla Valle AZ, Iriti M, Faoro F, Berti C, Ciappellano S. Department of Food Science and Microbiology (DISTAM), Section of Human Nutrition, University of Milan, Milan, Italy.

Intestinal uptake of abnormal prion protein (PrP(Sc)), the pathological agent involved in transmissible spongiform encephalopathies (TSEs), has been investigated in rainbow trout (Oncorhynchus mykiss). Experimental procedures were conducted in vivo by immunohistological PrP(Sc) localization in intestine and pyloric caeca after forced feeding of infected material. Results indicate that PrP(Sc) was absorbed by the intestinal mucosa and that it persisted in the fish gastrointestinal tract for up to 3 days in pyloric caeca and for up to 7 days in the distal intestine. It did not remain longer than 15 days in the fish intestine; furthermore, it did not cross the intestinal barrier.

PMID: 18377582 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/pubmed/18377582?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Results indicate that PrP(Sc) was absorbed by the intestinal mucosa and that it persisted

in the fish gastrointestinal tract for up to 3 days in pyloric caeca and for up to 7 days in the

distal intestine.

It did not remain longer than 15 days in the fish intestine;

WOULD this not be a potential risk factor for transmission of the PrPSc agent to cattle and other species via fish by-products and or fish feed ???


vCJD in the USA * BSE in U.S.

15 November 1999

snip...

Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows.

***I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing.

It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.

snip...

full text ;

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


http://madcowspontaneousnot.blogspot.com/2008/04/in-vivo-prion-protein-intestinal-uptake.html


Research article

Scrapie infectivity is quickly cleared in tissues of orally-infected farmed fish

Loredana Ingrosso1 , Beatriz Novoa2 , Andrea Z Dalla Valle3 , Franco Cardone1 , Raquel Aranguren2 , Marco Sbriccoli1 , Simona Bevivino1 , Marcello Iriti4 , Quanguo Liu1 , Vito Vetrugno1 , Mei Lu1 , Franco Faoro4 , Salvatore Ciappellano3 , Antonio Figueras2 and Maurizio Pocchiari1

1 Istituto Superiore di Sanità, Department of Cellular Biology and Neuroscience, viale Regina Elena,299,00161 Rome, Italy

2 Instituto Investigaciones Marinas, CSIC, Eduardo Cabello 6, 36208 Vigo, Spain

3 Section of Human Nutrition, Department of Food Science and Microbiology, DiSTAM, University of Milan, via Celoria 2, 20133 Milano, Italy

4 Institute of Plant Pathology, University of Milan and Institute of Plant Virology, CNR, Milano, Italy

author email corresponding author email

BMC Veterinary Research 2006, 2:21doi:10.1186/1746-6148-2-21

Published: 15 June 2006

Abstract Background Scrapie and bovine spongiform encephalopathy (BSE) belongs to the group of animal transmissible spongiform encephalopathy (TSE). BSE epidemic in the UK and elsewhere in Europe has been linked to the use of bovine meat and bone meals (MBM) in the feeding of cattle. There is concern that pigs, poultry and fish bred for human consumption and fed with infected MBM would eventually develop BSE or carry residual infectivity without disease. Although there has been no evidence of infection in these species, experimental data on the susceptibility to the BSE agent of farm animals other than sheep and cow are limited only to pigs and domestic chicken. In the framework of a EU-granted project we have challenged two species of fish largely used in human food consumption, rainbow trout (Oncorhynchus mykiss) and turbot (Scophthalmus maximus), with a mouse-adapted TSE strain (scrapie 139A), to assess the risk related to oral consumption of TSE contaminated food. In trout, we also checked the "in vitro" ability of the pathological isoform of the mouse prion protein (PrPSc) to cross the intestinal epithelium when added to the mucosal side of everted intestine.

Results Fish challenged with a large amount of scrapie mouse brain homogenate by either oral or parenteral routes, showed the ability to clear the majority of infectivity load. None of the fish tissues taken at different time points after oral or parenteral inoculation was able to provoke scrapie disease after intracerebral inoculation in recipient mice. However, a few recipient mice were positive for PrPSc and spongiform lesions in the brain. We also showed a specific binding of PrPSc to the mucosal side of fish intestine in the absence of an active uptake of the prion protein through the intestinal wall.

Conclusion These results indicate that scrapie 139A, and possibly BSE, is quickly removed from fish tissues despite evidence of a prion like protein in fish and of a specific binding of PrPSc to the mucosal side of fish intestine.

http://www.biomedcentral.com/1746-6148/2/21/abstract/


re-Scrapie infectivity is quickly cleared in tissues of orally-infected farmed fish Terry Singeltary (20 June 2006) http://disc.server.com/Indices/167318.html


>>>However, a few recipient mice were positive for PrPSc and spongiform lesions in the brain. We also showed a specific binding of PrPSc to the mucosal side of fish intestine in the absence of an active uptake of the prion protein through the intestinal wall. <<<


WOULD this not be further evidence to show that the rendering of such product after ingesting TSE tainted product, would further expose species that consume such product, i.e. even if the fish do not contract a TSE, could not the intestines and the feed that may still be there further expose species eating those by-products ???

Competing interests

none

http://www.biomedcentral.com/1746-6148/2/21/comments



An evolutionary basis for scrapie disease: identification of a fish prion mRNA

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Eric Rivera-Milla, Claudia A. O. Stuermer and Edward Málaga-Trillo

Department of Biology, University of Konstanz, 78457, Konstanz, Germany

Available online 11 December 2002.

Abstract Infectious prion proteins cause neurodegenerative disease in mammals owing to the acquisition of an aberrant conformation. We cloned a Fugu rubripes gene that encodes a structurally conserved prion protein, and found rapid rates of molecular divergence among prions from different vertebrate classes, along with molecular stasis within each class. We propose that a directional trend in the evolution of prion sequence motifs associated with pathogenesis and infectivity could account for the origin of scrapie in mammals.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCY-47DT7P2-2&_user=10&_coverDate=02%2F28%2F2003&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=3d43807a415e4a003c74b16fb8ae30e6



http://www.nature.com/news/2003/030131/full/news030127-12.html#B1




AS the crow flies, so do TSE...feces

Could Crows Play a Role in Spreading CWD was presented by Dr. Kurt VerCauteren, NWRC, WS-APHIS- USDA. From the first observations (40 years ago) of CWD in mule deer (Odocoileus hemionus) and Rocky Mountain elk (Cervus elaphus nelsoni) in Northern Colorado, the disease has been identified in an increasing geographic area. Mechanisms for the spread of CWD are incompletely understood. Birds have been identified as potential vectors for a number of diseases, where infected material is ingested and the disease agent is later shed in new areas after flying substantial distances. We hypothesized that avian scavengers have the potential to disseminate prions associated with transmissible spongiform encephalopathies (TSEs), like CWD, by a similar process. As prions are resistant to destruction, it is reasonable that infectious material could pass through the digestive tract of scavenging birds. Our objective was to determine if TSE-positive brain material from mice (i.e., mouse-adapted scrapie) could pass through the digestive tract of American crows (Corvus brachyrhynchos) and still be infectious to mice. Our experimental design included treatment groups of mice inoculated intraperitoneally with: 1) normal mouse brain, 2) infected mouse brain, 3) gamma-irradiated feces from crows gavaged with normal mouse brain, and 4) gamma-irradiated feces from crows gavaged with infected mouse brain. Our preliminary results indicate feces from each of 20 crows gavaged with infected mouse brain were infectious for mice (proportion of crows=1.00, 95% CI: 0.83-1.00) and average longevity for mice was 213 days (95% CI: 210-216). Longevity of mice inoculated with infected mouse brain was slightly less (198 days, 95% CI: 188-207). Most mice inoculated with normal brain, or feces from crows gavaged with normal brain, were still alive 1 year post inoculation with no evident clinical signs of TSE disease in any control mice. Our results demonstrate that a common, migratory North American scavenger, the American crow, can pass infective prions in feces and, therefore, could play a role in the spatial dissemination of prion disease.

http://www.usaha.org/committees/reports/2008/report-cwal-2008.pdf



Sunday, November 01, 2009

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

snip...

PLUS, this goes back to what the late Dr. Gibbs told me, and what the late Harash Narang book showed, Dr. Gibbs stating that the TSE agent could spread through the digestinal track, and survive, and could still have the potential to spread, and Harash Narang's book 'The Link', page 135, where a farmers around Kent have chickens with BSE. MAFF was aware of this and was suppose to do some studies? BUT, regardless whether or not these birds become clinical and die, the fact that the above studies showed that the TSE agent survived the digestinal tract, and went on to further infect mice via feces, is very disturbing, and further enhances transmission studies must be done asap. PLUS, this should be the final straw for chicken litter being fed back to cattle and other food producing animals for humans and animals. AND not to forget the Red Necked Ostrich and BSE? ...TSS


snip...


SEI805 Transmissibility of BSE to domestic fowl by injection with brain homogenate.

1 challenged bird died overnight (42 months p.i.) following a period of ataxia ­- histopathological examination pending. 2 further challenged birds are also showing neurological signs of ataxia and tremor (43 months p.i.). All affected birds are cock birds. The remaining 4 challenged hens are clinically normal (43 months p.i.).

2 control birds were culled due to intercurrent disease (40 and 43 months p.i.) . No significant lesions were observed in one and histopathological examination is pending on the other.

The remaining 6 control birds are clinically normal.

SE1806 Transmissibility of BSE to domestic fowl by oral exposure to brain homogenate.

1 challenged cock bird was necropsied (41 months p.i.) following a period of ataxia, tremor, limb abduction and other neurological signs. Histopathological examination failed to reveal any significant lesions of the central or peripheral nervous systems.

94/01.19/7.1

1 other challenged cock bird is also showing ataxia (43 months p.i.). The remaining 2 challenged cocks and 5 hens are clinically normal (43 months p.i.).

Ruther examinations are in progress to determine the cause of morbidity in these studies (SE1805 and SE1806).

For controls see SE1805.

snip...

94/01.19/7.1

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/01/19007001.pdf



also,

TRANSLATION

F437/91

A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY -

* The Red-Neck Ostrich 'THE AUTOPSY' & TSEs

THE AUTOPSY

Date: Mon, 11 Jun 2001 16:24:51 -0700 Reply-To: Bovine Spongiform Encephalopathy Sender: Bovine Spongiform Encephalopathy From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs 'THE AUTOPSY'

snip...

A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY

http://collections.europarchive.org/tna/20080609175635/http://www.bseinquiry.gov.uk/files/sc/Seac10/tab06.pdf



OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER 2002

OPINION

1. Necrophagous birds as possible transmitters of BSE. The SSC considers that the evaluation of necrophagous birds as possible transmitters of BSE, should theoretically be approached from a broader perspective of mammals and birds which prey on, or are carrion eaters (scavengers) of mammalian species. Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons, eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could be considered possible vectors of transmission and/or spread of TSE infectivity in the environment. In view also of the occurrence of Chronic Wasting Disease (CWD) in various deer species it should not be accepted that domestic cattle and sheep are necessarily the only source of TSE agent exposure for carnivorous species. While some information is available on the susceptibility of wild/exotic/zoo animals to natural or experimental infection with certain TSE agents, nothing is known of the possibility of occurrence of TSE in wild animal populations, other than among the species of deer affected by CWD in the USA.

1 The carrion birds are animals whose diet regularly or occasionally includes the consumption of carcasses, including possibly TSE infected ruminant carcasses.

C:\WINNT\Profiles\bredagi.000\Desktop\Necrophagous_OPINION_0209_FINAL.doc


http://ec.europa.eu/food/fs/sc/ssc/out295_en.pdf



snip... see full text ;


http://chronic-wasting-disease.blogspot.com/2009/11/american-crows-corvus-brachyrhynchos.html



7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE; 1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,

Links

Click here to read

The neuropathology of experimental bovine spongiform encephalopathy in the pig.

Ryder SJ, Hawkins SA, Dawson M, Wells GA.

Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.

In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.

PMID: 10684682 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract



Title: Experimental Intracerebral and Oral Inoculation of Scrapie to Swine: Preliminary Report

Authors

Greenlee, Justin Kunkle, Robert Hamir, Amirali

Submitted to: American Association of Veterinary Laboratory Diagnosticians Publication Type: Abstract Publication Acceptance Date: November 5, 2005 Publication Date: November 5, 2005 Citation: Greenlee, J.J., Kunkle, R.A., Hamir, A.N. 2005. Experimental Intracerebral and Oral Inoculation of Scrapie to Swine: Preliminary Report [abstract]. Proceedings of the American Association of Veterinary Laboratory Diagnosticians 48th Annual Conference. P. 38.

Technical Abstract: Transmissible spongiform encephalopathies (TSEs, prion diseases) are chronic neurodegenerative diseases that occur in humans, cattle, sheep, goats, cervids, and a number of laboratory animal models. In a laboratory setting, the host range of a given TSE can be tested by inoculating animals with brain tissue from affected animals through various routes including oral and intracranial. There is no evidence of the natural occurrence of any form of TSE in the pig, but pigs have been shown to be susceptible to bovine spongiform encephalopathy (BSE) infection by multiple-route parenteral challenge. However, pigs orally exposed at eight weeks of age to large amounts of brain from cattle clinically affected with BSE did not support infection after seven years of observation. In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility. This study utilized 26 swine randomly divided into three groups: controls (n=6), oral inoculates (n=8), and intracranial inoculates (n=12). Brain homogenate (10%) derived from scrapie-affected sheep was given by a single intracranial injection of 0.75 ml or by oral inoculation of 15 ml on four consecutive days. Scrapie inoculum was derived from clinically ill sheep inoculated with material derived from 13 sheep in seven source flocks. A sample of this material was also inoculated back into sheep to assure infectivity. Necropsies were planned for six months post inoculation, at approximately the time the pigs were expected to reach market weight. Samples collected were examined microscopically after routine staining (hematoxylin and eosin) and staining by standard immunohistochemical methods for prion protein (PrP**Sc). After approximately six months incubation time, no histologic lesions suggestive of spongiform encephalopathy or immunohistochemical evidence of prion infection were obtained. No evidence of scrapie infection was demonstrated in this short-term study, but positive results after an incubation period of only six months would be uncharacteristic. The only TSE with an incubation of six months or less known at this time is transmissible mink encephalopathy in mink, skunk, or raccoon hosts. However, scrapie in the raccoon model has a two-year incubation period. A replicate of littermate pigs has been inoculated and will be studied after long-term (3-7 years) incubation, and a similar study is underway with pigs inoculated with material derived from elk, mule deer, and whitetail deer affected by chronic wasting disease (CWD).

Last Modified: 03/19/2006

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=180786



EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE

2. It was agreed that there was evidence of scrapie in sheep as a result of food borne exposure. This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. As the working hypothesis is that there has been recycling of infected cattle tissues which has augmented the epidemic in cattle the continued infection of sheep with the BSE agent, via the food born source, cannot be excluded. There is therfore also a possibility that the BSE agent may have become endemic in the sheep population, but is is impossible to design any short-term research programme to elucidate this. ...

http://web.archive.org/web/20030517224223/http://www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf



Sunday, April 18, 2010

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html



AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.

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http://collections.europarchive.org/tna/20080102185948/http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf


http://caninespongiformencephalopathy.blogspot.com/



FELINE SPONGIFORM ENCEPHALOPATHY FSE

http://felinespongiformencephalopathyfse.blogspot.com/



STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

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To minimise the risk of farmers' claims for compensation from feed compounders.

To minimise the potential damage to compound feed markets through adverse publicity.

To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.

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THE FUTURE

4..........

MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...

SEE full text ;

http://collections.europarchive.org/tna/20080102153800/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf




THIS is what happens when you have the industry run the government, and if you think anything has changed in the last 2 decades, well you better think again, junk science and trade policy still rule the day $$$


TSS



BSE ATYPICAL USA

http://bse-atypical.blogspot.com/


SCRAPIE USA (over 20+ strains)

http://scrapie-usa.blogspot.com/


NOR-98 ATYPICAL SCRAPIE

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


Chronic Wasting Disease CWD (two strains documented to date)

http://chronic-wasting-disease.blogspot.com/


Transmissible Mink Encephalopathy TME (two strains documented to date)

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


PORCINE SPONGIFORM ENCEPHALOPATHY PSE

http://madporcinedisease.blogspot.com/


FELINE SPONGIFORM ENCEPHALOPATHY FSE

http://felinespongiformencephalopathyfse.blogspot.com/


Equine Spongiform Encephalopathy

http://equinespongiformencephalopathy.blogspot.com/


CANINE SPONGIFORM ENCEPHALOPATHY

http://caninespongiformencephalopathy.blogspot.com/


CREUTZFELDT JAKOB DISEASE

http://creutzfeldt-jakob-disease.blogspot.com/



TSS

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