Sunday, December 28, 2014

Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION aka BSE MAD COW TYPE DISEASE December 2014

Sent: Friday, December 26, 2014 1:37 PM
Subject: Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION aka BSE MAD COW TYPE DISEASE December 2014

Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION aka BSE MAD COW TYPE DISEASE December 2014
Greetings Honorable Phyllis K. Fong Inspector General United States Department of Agriculture, Honorable Gil H. Harden Deputy Assistant Inspector General for Audi OIG,  FSIS, APHIS, USDA, et al,
this is a reverse freedom of information request, that you did not request, but I thought I would issue the information back to you under the atypical rFOIA order.
over the past two decades, I have requested a few FOIA myself, so I thought I would send one back at ya, even though you did not ask. I hope it is very informative for you all.
this rFOIA order consists on the Transmissible Spongiform Encephalopathy TSE Prion Disease, all strains and variants in all species, and or any friendly fire therefrom i.e. IATROGENIC TSE. TSE Prion disease will also include the Alzheimer, Betaamyloids, Tauopathies, Proteinopathies, early onset dementia, for education use. it’s all fascinating to me, as crazy as that may be. as a layperson, I send this r-FOIA and the science and history that is enclosed in hopes someone will read it, and maybe see that the infamous ;
‘’US has 'triple firewall' against BSE, says NCBA leader’’ AND OR ‘’AMI official said the nation's freedom from BSE is a result of the "triple firewall strategy," consisting of import barriers, feed controls, and cattle testing.’’ ...END
WAS ALL, nothing but ink on paper.
my mother died from the Heidenhain Variant of Creutzfeldt Jakob disease on December 14, 1997, and I damn near died from MRSA at the end of 2001. so the end product of this are as follows.
I just don’t like prions, e-coli, listeria, feces, urine, or any dangerous pathogens, especially the TSE prion aka mad cow disease, and or antibiotics and or hormones, on or in the meat I eat. friendly fire, i.e. second hand transmission, i.e. iatrogenic TSE prion disease, from consumption of animal TSE prion disease, has a potential huge role in the further transmission of the TSE prion disease via the medical, surgical, dental, blood, tissue, organ transplant fields.
I am thinking of retiring at the end of 2014, you will miss me Winking smile 
but remember this, I am a meat eater. I don’t hate farmers, ranchers, cattle, sheep, cervid industry. I hate stupid, and I hate greed. I believe my mother was killed due to those reasons i.e. stupid and greed 17 years ago, and she was/is not the only one. ...GOOD LUCK!
p.s., hopefully, someone will forward this to the Honorable President of the United States of America, President Obama. ...kind regards, terry
rFOIA USDA/APHIS/FSIS as follows ;
FIRST, a review, a reminder of what the industry and FSIS USDA et al have said in the past about the BSE TSE prion, and about sporadic CJD’s, 85%+ of all human prion disease, which is rising in numbers, which has no known cause
From the very beginning the U.S. launched efforts to protect its cow herd from BSE.
• In 1989, the United States instituted an import ban on live animals, beef and beef products, such as meat and bone meal, from any country known to have BSE;
• In 1990, the U.S. government launched an aggressive surveillance program – the first of its kind by a country without BSE within its borders. By 2003, this level of surveillance was 47 times higher than international standards;
• Since 1990 cattle showing signs of neurological disorder have not been processed for human consumption;
• In 1997, the U.S. Food and Drug Administration mandated a feed ban prohibiting the use of feed supplements in cattle containing byproducts such as meat and bone meal from cattle and other animals The U.S. was the first country to institute such a ban;
• This “triple firewall” is reinforced by the common practice in the U.S. of harvesting the vast majority of cattle before the age of 24 months; BSE is more likely to occur in animals older than 30 months. (In fact, even in Europe, where BSE has reached epidemic proportions, of 1.6 million animals less than 30 months of age tested in 2002 there was not one positive case.)
Sporadic CJD and vCJD differ in that each has its own unique clinical features. Sporadic CJD was first identified in the 1920s and has a worldwide incidence of about one case per million people each year. There is no evidence that sporadic CJD is caused by what a person eats.
McDonald's, Burger King and Wal-Mart Stores quickly said they did not believe they had received meat from the animal. And almost as soon as Ms. Veneman finished her news conference, officials of the National Cattlemen's Beef Association began a conference call to seek to reassure consumers. Terry Stokes, chief executive of the group, referred to a "triple firewall" to prevent the introduction or spread of the disease.
Release No. 0203.05 Contact: Office of Communications (202) 720-4623 REMARKS AS PREPARED FOR DELIVERY By Acting Administrator, Dr. Barbara Masters The Food Safety and Inspection Service U.S. Department of Agriculture BSE Roundtable The University of Minnesota St. Paul, Minnesota June 9, 2005 Introduction
Good morning everyone. Today, I will focus my remarks on the public health aspects of BSE.
The Food Safety and Inspection Service (FSIS) uses science-based policies to effectively protect the health and well being of consumers worldwide against the threat of BSE and other food safety threats. Science-based policies are built on the public health model, which includes: assessment, policy development and assurance, or verification of effectiveness.
Historical Perspective
For more than a decade, the U.S. Department of Agriculture has had an aggressive program in place for surveillance, detection, and response to BSE. This program is led by APHIS, which has the responsibility for the health of live animals.
FSIS plays a strong role in the identification of samples from high-risk animals for this program. FSIS has over 7,500 inspection personnel in approximately 6,300 slaughter or processing establishments each and every day verifying the safety of meat, poultry and egg products. This includes identification and condemnation of cattle showing central nervous system symptoms on ante-mortem inspection.
The authority to monitor and enforce the animal feed ban rests with the Food and Drug Administration.
Our actions involved extensive collaboration among our agencies. Together we implemented regulatory actions and policy changes to create multiple firewalls to strengthen and protect against the introduction and spread of BSE in U.S. cattle and against human exposure to the BSE agent.
The detection of a single case of BSE in a cow imported from Canada on December 23, 2003 led us to further strengthen our BSE safeguards to protect human health.
I will now focus on FSIS' BSE measures that were taken following that finding.
On December 30, 2003, one week after the announcement of the positive BSE animal, then Secretary of Agriculture Ann Veneman, made a major policy announcement--the prohibition of the slaughter of non-ambulatory disabled cattle from the food supply, the removal of Specified Risk Materials from the food supply, as well as other actions to protect human and animal health.
Ban on Non-Ambulatory Disabled Cattle
USDA immediately put the ban on non-ambulatory disabled cattle into effect. These animals were considered unfit for human food.
FSIS' public health veterinarians are responsible for enforcing this ban, and we have provided them with training on when cattle are to be condemned at slaughter.
Following USDA's ban on non-ambulatory disabled cattle, FSIS issued four Federal Register documents, three rules and one notice.
These regulations were published within 20 days after the positive finding in Washington State. The process for publishing such rules normally would have taken several months to years.
FSIS had already done considerable work that laid the groundwork for these interim final rules. Several proactive measures had already been implemented to safeguard our beef supply not only for U.S. consumers but for our trading partners around the world.
Using science as a foundation, based in part on the Harvard-BSE risk assessment, we were able to take immediate action. This risk assessment reviewed available scientific information related to BSE and other TSEs; assessed pathways by which BSE could potentially occur in the United States and identified measures that could be taken to protect human and animal health in the United States.
The key findings of the Harvard BSE risk assessment were used in conjunction with the most current scientific literature and information from the BSE epidemic in the United Kingdom and elsewhere in Europe. This information was used to develop the interim final rules to address the food safety concerns arising from the finding of BSE in the United States.
I will now briefly summarize the interim final rules.
Test and Hold
First, FSIS issued a notice providing that any animals that are tested for BSE will not be marked as "inspected and passed" until our public health veterinarian receives confirmation that the cattle have, in fact, tested negative for BSE. We are referring to this as the "test-and-hold" policy.
Specified Risk Materials
FSIS published a second document, an interim final rule, to require that "specified risk materials" or SRMs from cattle do not enter the food supply.
We identified the brain, skull, eyes, trigeminal ganglia, spinal cord, central portions of the vertebral column and dorsal root ganglia of cattle 30 months of age and older as SRMs. Additionally we declared the tonsils and distal ileum of all cattle as SRMs. All SRMs are prohibited for use as human food.
This list of SRMs is consistent with international guidelines and actions taken by Canada. FDA took a similar action with the foods they regulate.
Banning SRMs from the food supply represents the most effective firewall for protecting public health.
Advanced Meat Recovery
The second rule involved product produced using advanced meat recovery (AMR). FSIS had previously established and enforced regulations that prohibit spinal cord from being included in AMR products labeled as "meat."
This rule expanded that prohibition to include dorsal root ganglia, or DRG. DRG are clusters of nerve cells along the vertebral column, in addition to the spinal cord tissue. Also, because the vertebral column and skull in cattle 30 months and older are considered inedible, we do not allow them to be used in processing Advance Meat Recovery products.
Banning Air-Injection Stunning
Finally, the third rule banned air-injection stunning equipment. This was done to ensure that portions of the brain are not dislocated into the tissues of the carcass as a consequence of stunning cattle during the slaughter process.
While the use of this type of stunning device is not common, officially banning its use not only ensures that it will be prohibited domestically, but will also make it a requirement for equivalency in establishments outside the United States when slaughtering for export to the U.S.
Summary of Actions
The actions I just reviewed are all science-based measures, designed to further minimize potential human exposure to the BSE agent through the consumption of beef and beef food products.
In addition to these actions, FSIS began collecting and submitting samples from ante-mortem condemned cattle to the APHIS enhanced surveillance program.
Stakeholder Feedback
To allow interested parties and stakeholders the opportunity to comment on the additional regulatory and policy measures under consideration FSIS, APHIS, and FDA published a joint advance notice of proposed rulemaking, or ANPR, to inform the public about what these agencies plan for keeping BSE out of the U.S.
Each agency laid out questions to solicit feedback. FSIS specifically sought comments on whether a country's BSE status should be taken into account when determining whether a country's meat inspection system is equivalent to the U.S. regulations including the provisions in the FSIS interim final rules.
In addition to the more than 22,000 comments we received, to help finalize our BSE rules, we will be reviewing data from APHIS' enhanced BSE surveillance program once it is completed. Additionally, we will review data from the updated Harvard BSE Risk Assessment that is being revised to evaluate the impacts of the FSIS interim final rules.
In the interim, through these rules-Banning Non-Ambulatory Disabled Cattle; Removing Specified Risk Materials; and Banning Air-Injection Stunning- in concert with FDA's feed ban and APHIS' surveillance program, FSIS is confident that we have an effective system, which protects public health.
The single BSE case in the United States led to changes and reevaluations of food safety system across our country.
It also led to an opportunity to build upon the strong partnerships we have with our sister agencies, APHIS, FDA, and other organizations.
Together, we must continue to rely on science-based solutions to prevent BSE from affecting animal and public health.
suppressed peer review of Harvard study October 31, 2002
MIND you the Harvard BSE risk ass. was partially funded by the very industry it was assessing.
ABOUT 132 pages;
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
1) The H-T BSE study authors have done their best to incorporate the existing data in their estimates of the parameters selected for inclusion in the model. Not much hard data exist that could be used directly for setting parameter values. Therefore, the authors used indirect data to justify logical arguments for setting a parameter to a particular range of values. The authors may have included some factors in their model simply because some indirect data could be found.
The reviewers had concerns that the importance of some parameters has been overestimated and others underestimated.
2) A rather optimistic choice was made in case of doubt or insufficient hard evidence or data. These concerns relate to overall model weaknesses in the general comments section. In the summary section, on Pages 98 and 99, several of the main issues that involve assumptions that cannot be verified with confidence are discussed, and several of them could serve as perfect examples of what has been argued here, that optimistic choices for favorable
Section 3 Identification of Data and Critical Evaluation of Evidence outcome or reassuring nuances are presented (e.g., the implementation rates, the remote chance that an infected animal had been imported from the UK ).
Reviewers commented on the import of MBM.
3) The UK export statistics mention a shipment of 20 tons to the U.S. in 1989. Such a quantity was enough to spark the Swiss epidemic. This part of import risk was considered negligible probably because the U.S. authorities could not corroborate this figure. The statement (Page 22, second paragraph, last sentence) that overseas shipping of MBM was economically noncompetitive seems questionable because at least for the period when MBM was almost available for free in the UK, it did get all the way to South- East Asia in large quantities. Figures from Southern State Cooperative of recent years are moot in this respect.
A reviewer also commented on the import of live cattle from the UK.
4) Because the USDA reported that about half of the animals imported in the risk period did not really enter the food chain, these were considered to carry no risk (Section 3.4.3). The report does not provide details or evidence to support this statement. Other arguments regarding the potential risk of import of live cattle from the UK, such as animals not being from a BSE-infected farm, and BSE not being a recognized disease (Page iii, last paragraph), are questionable. Admittedly, not many were imported at the peak of the risk period.
5) With respect to rendering (Table 3-3, Page 61), two log reduction for atmospheric continuous rendering with added fat is optimistic. Also there is a doubt about the statement on Page 25 (Appendix 1, second paragraph, last sentence) that addition of fat increases the inactivation.
6) In Section on stunning, it is assumed for the base case that air-injected stunning is not used in the U.S., based on conversations with involved persons (Page 55, first paragraph, seventh line). However, it seems that the model is based on unlikely events such as air-injected stunning. Therefore, the model may be limited and may become obsolete. In Section (Page 56, second paragraph, last sentence), the assumption that stunners
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Final Report not using air injection never cause contamination of the blood (during exsanguination) with brain material needs to be modified. 7) The remark in Section 4.5 in the last line on Page 99 does not sound very scientific: exposure could not have been substantial because we did not see many cases, having in mind the German experience. About the level of achieved surveillance, more will follow.
8) In Section on plate waste, it is said to mainly contain vegetable material (third paragraph, second sentence), and vegetable protein must be added to give it the correct nutritional value. The major question is why one would not add mammalian protein here instead of vegetable?
9) A reviewer commented on ProbPassAM (Section 2.1.1, Appendix 1, Page 9). If it is their intent, the authors should specify that ProbPassAM is the probability that a BSE-infected animal, not just an animal, passes AM inspection. The authors state that the probability of an animal passing AM inspection is age dependent. They provide the references that were used to derive these estimates. Because BSE evolves slowly, their argument that BSE in older animals is more likely to be detected makes sense, but the age-dependent variation is for animals without clinical signs. Thus, the probabilities really represent the age-dependant chance occurrence that an infected animal passes. Variations in probabilities for the three age categories are minute (to third decimal, Appendix 1, Section 3.1.1, Page 38). The authors do not specify variation in ProbPassAM in animals with clinical signs by the actual clinical signs, where variation in the probability among animals is likely to be higher than variation among age categories. Therefore, it appears that in one instance the parameter is overestimated and in the other underestimated.
What is important from an inspection point of view is to pay greater attention to early signs of disease. The probabilities also do not reflect improvements in detection over the 20-year time span. If the 0.10 probability chosen by the authors is an average probability of passing infected animals with early signs and animals with late signs, perhaps it is appropriate. If it represents the probability of passing an infected animal in the later stages of disease, then the
Section 3 Identification of Data and Critical Evaluation of Evidence
Figure 3-1. Forrester (rate/state) Diagram to Depict Relationships between Population Parameters estimate is probably high, because the neurological signs would be obvious to an inspector.
10) Reviewers commented on the cattle population parameters (Appendix 3A). The output tables list epidemic statistics such as the numbers of cattle infected and the numbers infected exhibiting clinical signs. It appears that cattle population parameters were included in the model to simulate epidemic statistics, which is also suggested in Figure 3-1 of the H-T BSE study report. Cattle population parameters specified in the H-T BSE study report are ProbBirth, ProbDeath, and InitSize. From an epidemiological point of view, these variables can be used to estimate the size of the national herd, which can define cattle at risk, and transmission of prions, for instance between cow and calf, which can define spread. However, the authors do not define clearly how the population parameters affect the output. That is, the mathematical relationships, if there are any, among the population parameters. Figure 3-1 in the H-T BSE report is not sufficient in describing the relationships. The authors do not report the density-dependent process used. They might consider using Forrester (rate/state) diagrams to depict the relationships in an easy to understand figure. For instance, a simple way to convey to the reader the factors that affect the size of the cattle population might be as shown in Figure 3-1.
Population Birth Rate 0.0833 at Time t Death Rate
A rate that increases the population and a rate that decreases the population determine the size of the herd at a point in time. Then the authors can elaborate. For instance, the rate of increase is affected by the current age-specific size of the population at time t-1 and the birth rate. The rate at which the population decreases is affected by the death/slaughter rate. The number culled for slaughter (and other factors) affects the death rate.
3-7 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Final Report In Table 3.4.1, the natural death rate is age-specific (Appendix 1, Page 45). It should be reported that the unit for age is months, and that the values tabulated are for beef cattle. Overall, the units of measurement should be included in all tables. Throughout the report, the stage of production is not considered. For instance, the death rate is different for stocker cattle on pasture than for feedlot cattle and varies seasonally and geographically and certainly by producer. When should details such as these be included in the model and when should they be excluded? More rationale should be given for the variables selected and for those omitted.
Population parameters were important in the Great Britain outbreak because destroying infected animals served to reduce the incidence rate and disease spread. It is unclear how the population parameters are used in this model.
11) About maternal transmission, one reviewer noted the following. The parameters beginCalving and endCalving, the beginning and ending age when cows give birth, are defined in Appendix 1, Pages 10 and 11. They are included presumably to estimate maternal transmission of prions to offspring or perhaps to determine the period at which transmission could occur. However, the actual relationship among the variables is not described. Therefore, one would have to examine the computer code to understand the relationships. Again, the authors might consider depicting the relationship as shown in Figure 3-2.
ProbTrans is a probability that a new born calf becomes infected if the mother is infected and the mother has lived through at least a fixed fraction of her incubation period and its value is 0.1 (Appendix 1, Section 2.2.2, Page 10). The fixed fraction is specified by parameter and its value is 0.833 (Appendix 1, Section, Page 76). Therefore, it appears that probTrans is a conditional probability that can take on one of the two values, which might be depicted by a Warnier-Orr diagram that the authors could use as a means of making the relationship easier for the reader to understand:
Section 3 Identification of Data and Critical Evaluation of Evidence
Figure 3-2. Forrester Diagram to Depict Relationships for Begincalving and Endcalving Rate BSE Calves BSE Mom Transmit (ProbTrans) Moms Time since infected
[Fraction of incubation period > 0.833] {ProbTrans = 10% [Fraction of incubation period < 0.833] {ProbTrans = 0% If the condition within the square brackets [ ] is true, then the assignment to the right of the curly brace { is made. Also, the authors need to specify if the fraction is >0.833 or ?0.833. 12) Apparently, the incubation period for BSE is assigned a value between 0 and >130 months according to the probability distribution ClinicalDate (Appendix 1, Pages 73-76). It is assumed that although the table indicates >130 months, the highest value actually used was 130.
13) A few assumptions are based on data extrapolated from dairy cattle and beef cattle or other animals. Do the results sum over all types of cattle?
14) The number of cattle among which blood meal from a single slaughtered animal is divided is estimated as described in Section 2.3.1 (Appendix 1, Page 11). Apparently, the blood collected from individual animals at slaughter establishments is pooled. The authors calculate the expected amount of blood meal consumed by a dairy cow to determine the number of animals (88) fed by a single 4,000 lb batch of blood meal. It is not clear how this number is used along with estimates of blood meal consumption (Table 3.3.3, Appendix 1, Page 39) by each bovine type, gender, and age combination to estimate the number of cattle infected by blood. Also, the value for the number of animals fed by a single batch of
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Final Report blood meal is reported as 88 in Appendix 1, on Pages 11 and 23, but 89 in Appendix I, Page 66. Which of these two numbers is correct? Because the units in the output tables (Appendix 3A) are not given, it can only be a guess that the value for blood (in mode of infection) represents cattle numbers infected by blood. 15) One reviewer commented on the lack of emphasis on exposure routes. It is generally accepted that the highest risk for BSE is from
Z import of live cattle or MBM from a country with BSE;
Z an internal processing system that is incapable of reducing infectivity below a certain threshold level (mainly the rendering system); and
Z exposure of ruminants to the end products of the second way (be it purposely or accidental, by cross-contamination). Although it is commendable that all possible routes and potential risks are addressed, the emphasis could have been placed more on the above limited number of priority routes, instead of dwelling on sometimes highly theoretical routes. In other words, some of the reported unlikely infection routes are easily dismissed by the model with a simple statement, whereas others are investigated to a surprisingly deep level. This comment is also related to the general comment on complexity and level of detail.
The study apparently treats the scrapie transmission (Section 2.3.3, Page 23) and the spontaneous BSE case (Section 2.3.1, Page 21) at the same level as the above listed priority routes. Below we provide an example of this inconsistency with what is considered major risks.
It is stated that from 750,000 up to 2.5 million animals are imported annually from Mexico and Canada (Section, Page 22). However, the H-T BSE study report does not address what happens in Mexico in terms of MBM exposure. In general, the report says it was extremely unlikely that those animals posed a risk of introducing BSE in the U.S. Perhaps the imported animals do not pose any risk, but what if they had been fed contaminated starter ratios as calves in Mexico? Even if such animals would not live until patent clinical stages, they can introduce infectivity into the system. The Scientific Study Committee (SCC) concluded that this was an area for consideration (or concern) in the case of the U.S.
Section 3 Identification of Data and Critical Evaluation of Evidence 16) The third paragraph on Page iii discusses the risk presented by the 334 animals brought into the U.S. from the UK between 1980 and 1989. The text states: These animals were imported as breeding stock, not as beef or dairy breeding animals. This fact is likely to have reduced their potential for exposure to BSE before their export from the UK (fifth line). There is a misunderstanding here as discussed below.
The cattle exported from the UK have carried a greater risk of being infected by BSE than the other members of their natal cohorts that were not exported. An assessment based solely on the incidence in the home-based remnant of the cohort can therefore be misleading. The reason for this elevated risk is because the exported animals are more likely to have received commercial concentrate feed, especially beef breeds that had a much lower exposure to feedstuffs containing MBM. One reason for this was to ensure that they were in the best physical condition. Examples of this apparent differential risk for exported animals are the animals of the Saler breed, which was exported to Canada, and animals exported to Denmark and Germany. More generally, at the beginning of the clinical epidemic, pedigree dairy herds were disproportionally represented. Their exposure to MBM was relatively greater than for other commercial herds, because of showing animals and general traditions of managing such herds. Unfortunately a proportion of the early affected pedigree herds was the source of Friesian heifers for export to Portugal to restock after the Contagious Bovine Pleuropneumonia (CBPP) outbreak there.
17) The second paragraph in Section 2.1.1 on Page 6 describes transmission of TSE disease in the case of sheep-borne scrapie. It is stated that TSE transmission has been inked to the use of vaccines. There is not much evidence that a relatively crudely prepared louping ill vaccine has been associated with transmission. The evidence from the Italian outbreak is far from conclusive.
18) It would have been more correct if at least experimentally was inserted after transmitted in the second sentence of the second paragraph of Section 2.1.2. 19) With reference to Anderson et al. (1996), it is stated in Section 2.1.3, third paragraph, that the susceptibility of animals peaks at 1.31 years of age and then decreases based on back
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Final Report calculation of the BSE model. There not only is a slight misunderstanding of the Anderson paper, but also an error in this paper that unfortunately has never been amended.
The peak susceptibility quoted is not derived by a back calculation. However, it is derived from a research institute s cattle herd that had a very unusual feeding profile and this is the error. In Great Britain, exposure to feedstuffs containing MBM is relatively rare between 6 months of age and approximately 2 years when heifers start to calve. This error is perpetuated in the Woolhouse and Anderson (1997) paper, which is not a separate investigation (i.e., both papers are part of the same investigation). Moreover, it has not been possible to determine the profile of age-dependent susceptibility and whether it does occur. This would require a laboratory-based study because the natural feeding pattern throughout the first 2 years of the life of cattle in Great Britain precludes the necessary epidemiological analysis of this putative age-dependent susceptibility.
The synthesis of the current evidence on this aspect is important to the risk assessment. If there is an age-dependent susceptibility it is not absolute. That is, all ages are susceptible. The age at which cattle are exposed orally and parentally to the BSE agent in experimental challenges in Great Britain has been 4 months. This is the age at which calves would have achieved their maximum intake of commercial concentrate feedstuffs under Great Britain conditions. The results from the British attack rate study, involving oral exposure to varying amounts of brain tissue from terminal cases of BSE, has resulted in an incubation period/age at clinical onset distribution similar to that observed in naturally occurring cases. The epidemiological evidence from the epidemic in Great Britain is that age at exposure does not influence the incubation period. In the ninth line of the third paragraph, it is hypothesized that agerelated susceptibility is associated with permeability of the intestine to large protein. A reference to the hypothesis is required because the change in permeability of the bovine intestine with age does not explain the apparent age-dependent susceptibility. The quoted changes occur too early after birth.
In the second paragraph on Page 12, findings from the attack rate experiments are discussed for the dose of BSE agent. The
Section 3 Identification of Data and Critical Evaluation of Evidence researchers should have made themselves aware of the attack rate study conducted in Great Britain. The lowest dose in the original study (a follow-up study using lower doses is in progress) was 1g. The results of this study should have been included here. There appears to be some confusion here and therefore a concern that the researchers may not have made the best use of the research results available, which is a trap generally advised against in terms of interpretation and use of the results of the bovine pathogenesis study. Essentially, the researchers have assumed that all of the animals in the pathogenesis study, exposed to 100g brain orally, had an incubation period of 36 months. This is not true and probably arises from a lack of synthesis of the results from these two studies; the attack rate study, although initiated at the same time as the pathogenesis study, was the scoping study for the latter. The problem is that in the attack rate study the 10 animals were exposed to 100g brain orally. However, the same exposure dose used in the pathogenesis study had incubation periods that ranged from 33 to 61 months. It is not correct to assume that all of the pathogenesis study animals had the same relatively short incubation period. Therefore, the proportional calculation described in Section 2.10.1, Appendix 1 will produce conservative estimates of infectivity and underestimate this value.
20) Section 2.2.1 describes scrapie in sheep as one of the possible causes of the BSE epidemic in the UK. The section is a little muddled in that it starts discussing transmission of sheep scrapie between sheep and then goes on to the sheep scrapie origin. The latter is a little simplistic and half-hearted. Again, this section is a little short on primary references and reviews of considerations of the origin, for example Kimberlin (1997). The comment on the feeding of concentrates to calves not taking place other than in Great Britain except Australia (Page 14, last sentence) is not true. The EU-sponsored Great Britain exercise clearly indicated that the feeding of concentrates containing MBM to calves was not restricted to Great Britain/UK. Thus, there is a misquotation regarding the feeding of concentrates to calves, which needs to be corrected to make accurate international comparisons. Finally, the last sentence of Section 2.2.1 could be misinterpreted by the uninformed to mean that cattle are not susceptible to oral exposure to sheep scrapie. This is not true.
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Final Report
21) Section 2.2.2 discusses sporadic BSE as one of the possible causes for the UK epidemic. The first sentence of this section is rather vague and conflicting. Is this referring to relativity to all other countries or just to the U.S.? The evidence suggests that this is only true for the U.S. Occurrence of sporadic BSE according to age of cattle is discussed in the second paragraph. The age distributions of the UK animals are specifically mentioned. However, other European countries certainly have dairy cow populations with similar age distributions, which needs to be considered here.
22) As discussed in Section 2.2.3, toxic agents and other hypotheses as a possible cause of the BSE epidemic in the UK are discussed here. The other hypotheses may not deserve any great attention in such a risk assessment. They could have been dismissed either by reference to reviews by others such as the Spongiform Encephalopathy Advisory Committee (SEAC) in Great Britain or by the EU s SSC. As it stands, it is misleading. For example, the Organophosphate Pesticides hypothesis has not been a singular hypothesis. It has changed significantly throughout the epidemic by its protagonist. Also, in the last sentence in the first paragraph of Section, it is stated that resulting conditions from copper deficiency had signs and pathological changes similar to those of BSE, which is not true. Section discusses pituitary hormones, but the fact that transmission via hormones derived from bovine pituitaries was considered in the original epidemiological study has been ignored.
23) As discussed in Section, there is a theoretical risk that cattle could be exposed to a TSE from porcine-derived protein. One of the two potential sources of this exposure can be a natural TSE that infects pigs. Section discusses infectivity in pigs due to TSE infection. BSE in pigs, as a clinical disease or subclinical infection, has been a concern worldwide. They were clearly of potential importance in Great Britain because of the inclusion rate of MBM. In simple terms pigs could represent an effective sump for the BSE agent, in which the BSE agent is effectively removed from the feed system, or at the other extreme they could represent a means of amplification. The evidence from Great Britain could have perhaps been used to strengthen this section. This is so specifically for the last part of the second paragraph and the third paragraph on Page 29. Some
Section 3 Identification of Data and Critical Evaluation of Evidence evidence indicates that subclinical infection is not a problem in pigs, and this is not presented. Also, some evidence shows that clinical disease in pigs has not occurred in the pig population in Great Britain. This has probably got lost in various reports. However, if one assumes that the incubation period in pigs is the same as that for BSE in cattle and the surveillance for neurological disease in pigs in Great Britain is equally effective for such disease in cattle, then the number of expected cases in the pig population in Great Britain can be tens of thousands. On the first assumption there is no evidence to dismiss it. On the second assumption, evidence indicates that the surveillance of disease, including neurological disease, in pigs is more effective than in cattle in Great Britain.
BSE in pigs was detected by a neuropathologist whose specialism was neurological disease in pigs. Also, during the BSE epidemic outbreaks of neurological disease in pigs in Great Britain were detected, brought to the attention of MAFF scientists, and investigated. The main point is that the third paragraph on Page 29 has a touch of innumeracy. The percentage of pigs slaughtered at less than 6 months of age is not an important statistic compared to the number of pigs that reach a potentially susceptible age (~5 years), and this is what the analysis of the pig population referred to above was concerned with. There is really no evidence that pigs are important in the epidemiology of BSE, but quoting percentages rather than absolute numbers is not helpful in such an important risk assessment.
24) Actions taken in the UK to check BSE are described in Section 2.4.2, Page 37. The fifth sentence (line 7) indicates that the ban on specific bovine offal (SBO) as ingredients in feed stuff helps to identify tissues with the highest infectivity. It should be indicated that these high risk tissues were identified as a result of research on sheep scrapie. This sentence also could be more fully referenced. The last sentence of the paragraph is more accurate if it is moved to be the penultimate sentence. Because by 1997 the additional ban on the use of mammalian-derived protein in 1996 could not possibly have had any effect on the clinical incidence. To make the second paragraph more realistic, it may be noted that the SBO ban, with respect to the human food supply, was introduced in 1989 because of the knowledge that when the
Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Final Report
scrapie agent successfully crosses to another species, it can have altered transmission characteristics with respect to other species. Also, the tissues listed as the SBOs, such as brain and spinal cord from cattle older than 6 months, are incomplete. The chronology of events that is suggested in the third paragraph is not correct. The national surveillance for Creutzfeldt-Jakob Disease (CJD) was formally instigated in May 1990, which is clear from the CJD Surveillance Unit s website. In Table 2-2, the chronology of BSE-regulated actions in the UK contains errors. For example, there was no selective culling in 1990, and spinal cord in animals older than 6 months was included in the original SBO ban. There are perhaps some other important exclusions even though this is a summary table. For a detailed chronology, refer to the six monthly progress report on the BSE epidemic published by the Ministry of Agriculture, Fisheries, and Food (MAFF) (now the Department for Environment, Food, and Rural Affairs or DEFRA), which is available on their web site.
The two measures to prevent the BSE epidemic described in the last two paragraphs of this section are confused as different bans. The reality was that in March 1996, the SEAC s recommendation was for the deboning of carcasses of animals older than 30 months of age together with the removal of all obvious lymphatic and nervous tissues. This was not possible because of an insufficient number of deboning plants. The political decision was therefore made, at the Prime Ministerial level, to remove all animals over 30 months old from the human chain. The ban on bone-in-beef was introduced as a precautionary measure as a result of the later results from the BSE pathogenesis study (in cattle) conducted in Great Britain that suggested that infectivity may be present in dorsal root ganglia. 25) In Section 2.4.5, BSE surveillance in the U.S. was evaluated. The section reads as if there is a little complacency about the surveillance for BSE, and CJD/vCJD in the U.S. A more critical evaluation appears to be appropriate. There have clearly been a number of problems with surveillance for clinical BSE. The first is the general level of surveillance in the U.S. and other countries. The second is the fact that at low incidence BSE is clearly a difficult disease to identify because of its more behavioral, rather than neurological, clinical presentation in at least the early clinical phase and the rather variable clinical signs. Thirdly, a concentration on
Section 3 Identification of Data and Critical Evaluation of Evidence suspect rabies cases has not proved to be very effective within continental Europe; this is mainly because rabies is endemic in the less cattle-dense areas and such surveillance (on its own) can therefore exclude a significant proportion of the cattle population. Fourthly, downer cows are probably not the best targets for BSE surveillance.
The time frame of the BSE risk assessment work is not clear. The executive summary indicates a starting year of 1998 and the scientific references section contains some papers published in May 2001. An improved awareness of the extent and magnitude of the incidence of BSE in EU member states in continental Europe emerged towards the end of 2000. Any comment on the omission of what has been learned or stressed from this additional surveillance in Europe, arising from the use of the more rapid and economical tests described in Section 2.4.1, may be misplaced. However, two related aspects emerge. The first is that testing animals at slaughter improves quite dramatically our knowledge on the incidence of BSE in countries with a low incidence of clinical BSE and therefore a relatively poor awareness of the intricacies of the clinical picture. Secondly, targeting surveillance to the more general category of fallen stock/casualty slaughter animals, rather than just downer cows is a much more effective method.
A comparison of surveillance for CJD/vCJD in the U.S. with that in the UK and the more widely based EU funded surveillance project would have been helpful because there do seem to be some differences. A lack of change in the observed incidence of CJD in the U.S. could be interpreted as providing evidence of no increased intensity in surveillance. This comment is made in light of the findings from those countries that have participated in the international project on CJD surveillance.
Owens, Julie
From: Terry S. Singeltary Sr. []
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98
From: Terry S. Singeltary Sr.
Sent: Tuesday, December 23, 2014 9:25 AM
WASHINGTON, July 25, 2014 – As of July 1, there were 95.0 million head of cattle on U.S. farms, according to the Cattle report published today by the U.S. Department of Agriculture's National Agricultural Statistics Service (NASS). This is the lowest inventory for July 1 since the series began in 1973. ...
Bovine Spongiform Encephalopathy (BSE): Ongoing Surveillance Program Last Modified: Nov 25, 2014 Print Current Monthly Test Results
APHIS reports ongoing surveillance test totals monthly.
The BSE ongoing surveillance program will sample approximately 40,000 animals each year. Under the program, USDA will continue to collect samples from a variety of sites and from the cattle populations where the disease is most likely to be detected, similar to the enhanced surveillance program procedures.
Month Number of Tests November 2014 2,401 October 2014 1,386
Fiscal Year 2007-2014 Test Results
OIE Surveillance Points: design prevalence of 1 case per 100,000 U.S. adult cattle and 95% confidence; 300,000 OIE points over 7 years, or 42,857 OIE points on average per year are required.
BSurvE Surveillance Points: design prevalence of 1 case per 1,000,000 U.S. adult cattle and 95% confidence; 3,000,000 points over 7 years, or 428,571 BSurvE points on average per year are required.
Samples Tested, OIE Points, and BSurvE Points by Fiscal Year
Fiscal Year Number of Valid Tests OIE Points BSurvE Points FY 2014 41,291 678,622 1,642,452 FY 2013 43,173 1,048,554 2,505,042 FY 2012 42,202 1,066,637 2,523,447 FY 2011 40,482 997,360 2,344,436 FY 2010 44,301 948,593 2,233,643 FY 2009 44,217 1,036,849 2,442,400 FY 2008 43,145 1,121,624 2,677,665 FY 2007* 43,336 1,487,215 3,621,117
* FY2007 - first complete year of BSE Ongoing Surveillance
BSE Ongoing Surveillance Program Cumulative Totals
Valid Tests From September 1, 2006 to November 25, 2014: 345,934 OIE Points From September 1, 2006 to November 25, 2014: 8,443,289 BSurvE Points From September 1, 2006 to November 25, 2014: 20,130,647
(see "BSE Ongoing Surveillance Plan" for information on OIE and BSurvE points)
OAI 2014
OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.
1075 ATL-DO 3E+09 JP Green Milling Company, Inc. 496 East Depot St Mocksville NC 27028-2419 OPR DR, NL, TH HP ######## OAI Y
1580 ATL-DO 1035703 ISE Newberry Inc. DBA Newberry Feed 2431 Vincent St. Newberry SC 29108-0714 OPR DR, FL, NL, TH HP ######## OAI Y
CIN-DO 3E+09 Michael A Hatcher 307 Holmes Bend Rd., PO Box 517 Columbia KY 42728-0517 OPR FR NP 9/4/2014 OAI Y
DAL-DO 3.01E+09 Rusty Cattle Company 13893 Highway 133 Paul's Valley OK 73075-8595 OPR FR NP ######## OAI Y
DAL-DO 3.01E+09 Stonegate Farms 770 CR 1038 Muleshoe TX 79347 OPR FR NP ######## OAI Y
FLA-DO 1E+09 North Florida Holsteins, LLC. 2740 W County Road 232 Bell FL 32619-1350 OPR FR NP ######## OAI Y
MIN-DO 2115215 All American Coop 113 4th St Southeast Stewartville MN 55976 OPR DR, FL, TH NP 9/9/2013 OAI Y
NYK-DO 3.01E+09 James W. Michalek 1068 Clinton Street Rd Attica NY 14011-9711 OPR FR NP ######## OAI Y
NYK-DO 3.01E+09 Papas Dairy LLC 322 Wheeler Rd North Bangor NY 12966-2931 OPR FR NP 8/8/2014 OAI Y
NYK-DO 3.01E+09 Sherry Sammons 612 Stoner Trail Rd Fonda NY 12068-5007 OPR FR, OF NP ######## OAI Y
PLEASE NOTE, THE VAI BREACHES IN THE MAD COW FEED BAN ARE SO NUMEROUS (100s), I did not list them, you can search them out on the spread sheet url below ;
infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et al TRIPLE MAD COW FIREWALL, nothing but ink on paper. ...tss
Sunday, December 15, 2013
OAI 2012-2013
OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.
ATL-DO 1035703 Newberry Feed & Farm Ctr, Inc. 2431 Vincent St. Newberry SC 29108-0714 OPR DR, FL, FR, TH HP 9/9/2013 OAI Y
DET-DO 1824979 Hubbard Feeds, Inc. 135 Main, P.O. Box 156 Shipshewana IN 46565-0156 OPR DR, FL, OF DP 8/29/2013 OAI Y
ATL-DO 3001460882 Talley Farms Feed Mill Inc 6309 Talley Rd Stanfield NC 28163-7617 OPR FL, TH NP 7/17/2013 OAI N
NYK-DO 3010260624 Sherry Sammons 612 Stoner Trail Rd Fonda NY 12068-5007 OPR FR, OF NP 7/16/2013 OAI Y
DEN-DO 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N
CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y
*** DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N
Ruminant Feed Inspections Firms Inventory (excel format)
PLEASE NOTE, the VAI violations were so numerous, and unorganized in dates posted, as in numerical order, you will have to sift through them for yourselves. ...tss
Sunday, December 15, 2013
Tuesday, June 11, 2013
*** Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant deviations from requirements in FDA regulations that are intended to reduce the risk of bovine spongiform encephalopathy (BSE) within the United States
Thursday, June 6, 2013
since our fine federal friends have decided not to give out any more reports on the USA breaches of the feed ban and surveillance etc. for the BSE TSE prion mad cow type disease in the USDA livestock, I thought I might attempt it. I swear, I just don’t understand the logic of the SSS policy, and that includes all of it. I assure you, it would be much easier, and probably better for the FDA and the USDA INC., if they would simply put some kind of report out for Pete’s sake, instead of me doing it after I get mad, because I am going to put it all out there. the truth.
PLEASE BE ADVISED, any breach of any of the above classifications OAI, VAI, RTS, CAN lead to breaches into the feed BSE TSE prion protocols, and CAN lead to the eventual suspect tainted feed reaching livestock. please, if any USDA official out there disputes this, please explain then how they could not. paperwork errors can eventually lead to breaches of the BSE TSE prion mad cow feed ban reaching livestock, or contamination and exposure there from, as well.
I would sure like to see the full reports of just these ;
4018 CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y
9367 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N
9446 DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N
9447 DEN-DO 3002857110 Weld County Bi-Products dba Fort Morgan Pet Foods 13553 County Road 19 Fort Morgan CO 80701-7506 OPR RE HP 12/7/2011 OAI N
see full list of the fda mad cow bse feed follies, toward the bottom, after a short brief update on the mad cow bse follies, and our good friend Lester Crawford that was at the FDA.
ALSO, I would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters the fda use to put out for each violations. simply put, this excel format sucks, and the FDA et al intentionally made it this difficult to follow the usda fda mad cow follies. this is an intentional format to make it as difficult as possible to follow these breaches of the mad cow TSE prion safety feed protocols. to have absolutely no chronological or numerical order, and to format such violations in a way that they are almost impossible to find, says a lot about just how far the FDA and our fine federal friends will go through to hide these continued violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols there from. once again, the wolf guarding the henhouse $$$
Inspections conducted by State and FDA investigators are classified to reflect the compliance status at the time of the inspection, based upon whether objectionable conditions were documented. Based on the conditions found, inspection results are recorded in one of three classifications:
OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.
VAI (Voluntary Action Indicated) when inspectors find objectionable conditions or practices that do not meet the threshold of regulatory significance, but warrant an advisory to inform the establishment that inspectors found conditions or practices that should be voluntarily corrected. VAI violations are typically technical violations of the 1997 BSE Feed Rule. These violations include minor recordkeeping lapses or conditions involving non-ruminant feeds.
NAI (No Action Indicated) when inspectors find no objectionable conditions or practices or, if they find objectionable conditions, those conditions are of a minor nature and do not justify further actions.
when sound science was bought off by junk science, in regards to the BSE TSE prion mad cow type disease, by the USDA, CFIA, WHO, OIE, et al. $$$
when the infamous, and fraudulently USDA, FSIS, APHIS, FDA, gold card was taken away that infamous day in December of 2003, all cards were off the table, it was time to change the science, and change they did. ...tss
snip. ...please see full text ;
Thursday, June 6, 2013
Saturday, August 30, 2014
Maine Firm Recalls Ribeye and Carcass Products That May Contain Specified Risk Materials SRM TSE PRION aka mad cow type disease
Friday, December 19, 2014
Rancho Alleged Cancerous Eyeball Case Going To Trial
Thursday, November 28, 2013
Department of Justice Former Suppliers of Beef to National School Lunch Program Settle Allegations of Improper Practices and Mistreating Cows
seems USDA NSLP et al thought that it would be alright, to feed our children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high risk cattle for mad cow type disease, and other dangerous pathogens, and they did this for 4 years, that was documented, then hid what they did by having a recall, one of the largest recalls ever, and they made this recall and masked the reason for the recall due to animal abuse (I do not condone animal abuse), not for the reason of the potential for these animals to have mad cow BSE type disease (or other dangerous and deadly pathogens). these TSE prion disease can lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE NEXT 5 DECADES FOR CJD ???
Saturday, September 21, 2013
Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ??? this recall was not for the welfare of the animals. ...tss you can check and see here ; (link now dead, does not work...tss)
try this link ;
Sunday, November 13, 2011
*** California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock
Thursday, February 13, 2014
HSUS VS USDA ET AL BAN DOWNER CALVES FOR HUMAN CONSUMPTION (*veal) and potential BSE risk factor there from
Saturday, November 10, 2012
Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk Materials Nov 9, 2012 WI Firm Recalls Beef Tongues
Saturday, July 23, 2011
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009
Thursday, June 26, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials
Tuesday, July 1, 2008
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
Friday, August 8, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed
Saturday, April 5, 2008
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings
Friday, October 15, 2010
BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle
Thursday, November 18, 2010
Dustin Douglass was indicted and charged with making a fraudulent application to the VA, in an effort to obtain benefits from injuries Douglas represented he suffered while deployed in Iraq. Based on his application, the VA provided benefits totaling $22,148.53. Douglass claimed he suffered various injuries and illnesses as a result of his service in combat. The investigation revealed Douglass had, in fact, been deployed to Iraq, but had served as a computer specialist, had never been in combat, and did not suffer the service-related injuries and illnesses he claimed to have suffered. Douglass was placed on supervised release for 3 years, and required to pay $22,148.53 in restitution. Galen Niehues, an inspector for the Nebraska Department of Agriculture, (NDA), was convicted of mail fraud for submitting falsified reports to his employer concerning inspections he was supposed to perform at Nebraska cattle operations. Niehues was tasked with performing inspections of Nebraska ranches, cattle and feed for the presence of neurological diseases in cattle including Bovine Spongiform Encephalopathy (BSE), also known as “Mad Cow Disease”. Niehues was to identify cattle producers, perform on-site inspections of the farm sites and cattle operations, ask producers specific questions about feed, and take samples of the feed. Niehues was to then submit feed samples for laboratory analysis, and complete reports of his inspections and submit them to the NDA and to the Federal Food and Drug Administration (FDA). An investigation by the FDA and NDA revealed Niehues had fabricated approximately 100 BSE inspections and inspection reports. When confronted, Niehues admitted his reports were fraudulent, and that had fabricated the reports and feed samples he submitted to the NDA. Niehues received a sentence of 5 years probation, a 3-year term of supervised release, and was required to pay $42,812.10 in restitution.
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
Topics that will be covered in ongoing or planned reviews under Goal 1 include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
-MORE Office of the United States Attorney District of Arizona
FOR IMMEDIATE RELEASE For Information Contact Public Affairs
February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602) 525-2681
PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel Knauss stated, “The integrity of the system that tests for mad cow disease relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without that honest cooperation, consumers both in the U.S. and internationally are at risk. We want to thank the USDA’s Office of Inspector General for their continuing efforts to safeguard the public health and enforce the law.” Farm Fresh Meats and Farabee were charged by Information with theft of government funds, mail fraud and wire fraud. According to the Information, on June 7, 2004, Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S. Department of Agriculture (the “USDA Agreement”) to collect obex samples from cattle at high risk of mad cow disease (the “Targeted Cattle Population”). The Targeted Cattle Population consisted of the following cattle: cattle over thirty months of age; nonambulatory cattle; cattle exhibiting signs of central nervous system disorders; cattle exhibiting signs of mad cow disease; and dead cattle. Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per obex sample for collecting obex samples from cattle within the Targeted Cattle Population, and submitting the obex samples to a USDA laboratory for mad cow disease testing. Farm Fresh Meats further agreed to maintain in cold storage the sampled cattle carcasses and heads until the test results were received by Farm Fresh Meats.
Evidence uncovered during the government’s investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.
Evidence collected also demonstrated that Farm Fresh Meats and Farabee failed to maintain cattle carcasses and heads pending test results and falsified corporate books and records to conceal their malfeasance. Such actions, to the extent an obex sample tested positive (fortunately, none did), could have jeopardized the USDA’s ability to identify the diseased animal and pinpoint its place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee pleaded guilty to stealing government funds and using the mails and wires to effect the scheme. According to their guilty pleas:
(a) Farm Fresh Meats collected, and Farabee directed others to collect, obex samples from cattle outside the Targeted Cattle Population, which were not subject to payment by the USDA;
(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests to the USDA knowing that the requests were based on obex samples that were not subject to payment under the USDA Agreement;
(c) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Data Collection Forms to the USDA’s testing laboratory that were false and misleading;
(d) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Submission Forms filed with the USDA that were false and misleading;
(e) Farm Fresh Meats falsified, and Farabee directed others to falsify, internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats was seeking and obtaining payment from the USDA for obex samples obtained from cattle outside the Targeted Cattle Population; and
(f) Farm Fresh Meats failed to comply with, and Farabee directed others to fail to comply with, the USDA Agreement by discarding cattle carcasses and heads prior to receiving BSE test results. A conviction for theft of government funds carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud convictions carry a maximum penalty of 20 years imprisonment. Convictions for the above referenced violations also carry a maximum fine of $250,000 for individuals and $500,000 for organizations. In determining an actual sentence, Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide appropriate sentencing ranges. The judge, however, is not bound by those guidelines in determining a sentence.
Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The investigation in this case was conducted by Assistant Special Agent in Charge Alejandro Quintero, United States Department of Agriculture, Office of Inspector General. The prosecution is being handled by Robert Long, Assistant U.S. Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee) # # #
WE can only hope that this is a single incident. BUT i have my doubts. I remember when the infamous TOKEN Purina Feed Mill in Texas was feeding up to 5.5 grams of potentially and probably tainted BANNED RUMINANT feed to cattle, and the FDA was bragging at the time that the amount of potentially BANNED product was so little and the cattle were so big ;
"It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated."
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed. ... FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
WE now know all that was a lie. WE know that literally Thousands of TONS of BANNED and most likely tainted product is still going out to commerce. WE know now and we knew then that .005 to a gram was lethal. WE know that CWD infected deer and elk, scrapie infected sheep, BSE and BASE infected cattle have all been rendered and fed back to livestock (including cattle) for human and animal consumption.
Paul Brown, known and respected TSE scientist, former TSE expert for the CDC said he had ''absolutely no confidence in USDA tests before one year ago'', and this was on March 15, 2006 ;
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."
OR, what the Honorable Phyllis Fong of the OIG found ;
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
Table 1. Animal feed ingredients that are legally used in U.S. animal feeds
Rendered animal protein from Meat meal, meat meal tankage, meat and bone meal, poultry meal, animal the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell production animals and other meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal animals digest from dead, dying, diseased, or disabled animals including deer and elk Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and undried processed animal waste products
Food-animal production in the United States has changed markedly in the past century, and these changes have paralleled major changes in animal feed formulations. While this industrialized system of food-animal production may result in increased production efficiencies, some of the changes in animal feeding practices may result in unintended adverse health consequences for consumers of animal-based food products. Currently, the use of animal feed ingredients, including rendered animal products, animal waste, antibiotics, metals, and fats, could result in higher levels of bacteria, antibioticresistant bacteria, prions, arsenic, and dioxinlike compounds in animals and resulting animal-based food products intended for human consumption. Subsequent human health effects among consumers could include increases in bacterial infections (antibioticresistant and nonresistant) and increases in the risk of developing chronic (often fatal) diseases such as vCJD. Nevertheless, in spite of the wide range of potential human health impacts that could result from animal feeding practices, there are little data collected at the federal or state level concerning the amounts of specific ingredients that are intentionally included in U.S. animal feed. In addition, almost no biological or chemical testing is conducted on complete U.S. animal feeds; insufficient testing is performed on retail meat products; and human health effects data are not appropriately linked to this information. These surveillance inadequacies make it difficult to conduct rigorous epidemiologic studies and risk assessments that could identify the extent to which specific human health risks are ultimately associated with animal feeding practices. For example, as noted above, there are insufficient data to determine whether other human foodborne bacterial illnesses besides those caused by S. enterica serotype Agona are associated with animal feeding practices. Likewise, there are insufficient data to determine the percentage of antibiotic-resistant human bacterial infections that are attributed to the nontherapeutic use of antibiotics in animal feed. Moreover, little research has been conducted to determine whether the use of organoarsenicals in animal feed, which can lead to elevated levels of arsenic in meat products (Lasky et al. 2004), contributes to increases in cancer risk. In order to address these research gaps, the following principal actions are necessary within the United States: a) implementation of a nationwide reporting system of the specific amounts and types of feed ingredients of concern to public health that are incorporated into animal feed, including antibiotics, arsenicals, rendered animal products, fats, and animal waste; b) funding and development of robust surveillance systems that monitor biological, chemical, and other etiologic agents throughout the animal-based food-production chain “from farm to fork” to human health outcomes; and c) increased communication and collaboration among feed professionals, food-animal producers, and veterinary and public health officials.
Sapkota et al. 668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health Perspectives
snip...see full text ;
Sunday, December 15, 2013
Thursday, July 24, 2014
Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse
LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow. This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$ ALABAMA MAD COW g-h-BSEalabama In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)
her healthy calf also carried the mutation
(J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009
Owens, Julie
From: Terry S. Singeltary Sr. []
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98
infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et al TRIPLE MAD COW FIREWALL, 10 YEARS AFTER ;
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.
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.
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Final Feed Investigation Summary - California atypical L-type BSE Case - July 2012
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Scrapie from sheep could infect humans with 'mad cow disease', study finds
Tuesday, December 2, 2014
UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease
USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE WORLD (?) [protected by the BSE MRR policy] $$$
Monday, December 1, 2014
Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review December 1, 2014
Friday, November 28, 2014
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
Friday, December 5, 2014
***SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide
(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,
Tuesday, December 23, 2014
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).
as I said, what if ?
*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
Saturday, April 19, 2014
Exploring the zoonotic potential of animal prion diseases: In vivo and in vitro approaches
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.
Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other species
there is in fact evidence that the potential for cwd transmission to humans can NOT be ruled out.
I thought your readers and hunters and those that consume the venison, should have all the scientific facts, personally, I don’t care what you eat, but if it effects me and my family down the road, it should then concern everyone, and the potential of iatrogenic transmission of the TSE prion is real i.e. ‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there deer antler velvet and TSE prions and nutritional supplements there from, all a potential risk factor that should not be ignored or silenced. ...
the prion gods at the cdc state that there is ;
''no strong evidence''
but let's see exactly what the authors of this cwd to human at the cdc state ;
now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS (
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
Sent: Sunday, September 29, 2002 10:15 AM
To:;; ebb8@CDC.GOV
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
full text ;
***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and venison and lamb**************
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.
Tuesday, November 04, 2014
*** Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011
Thursday, March 20, 2014
Tuesday, July 01, 2014
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets? ***
Thursday, October 23, 2014
Tuesday, October 21, 2014
*** Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” 26.
Sunday, January 06, 2013
*** "it‘s no longer its business.”
Sunday, July 13, 2014
Louisiana deer mystery unleashes litigation 6 does still missing from CWD index herd in Pennsylvania Great Escape
Saturday, June 29, 2013
Tuesday, June 11, 2013
*** CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania
Wednesday, September 04, 2013
***cwd - cervid captive livestock escapes, loose and on the run in the wild...
Tuesday, October 07, 2014
*** Wisconsin white-tailed deer tested positive for CWD on a Richland County breeding farm, and a case of CWD has been discovered on a Marathon County hunting preserve
Thursday, October 02, 2014
*** IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
Tuesday, April 29, 2014
CWD Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose FR Doc No: 2014-09714 April 29, 2014 UPDATE
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
28 Mar 01
Like lambs to the slaughter
31 March 2001
by Debora MacKenzie Magazine issue 2284.
FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.
As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.
But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.
Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.
Monday, December 1, 2014
Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review December 1, 2014
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
Tuesday, July 21, 2009
Transmissible mink encephalopathy - review of the etiology
Saturday, December 01, 2007
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model
Sunday, December 10, 2006
Transmissible Mink Encephalopathy TME
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease
Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease
Sunday, May 18, 2008
Sunday, May 18, 2008
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
Sunday, May 18, 2008
Tuesday, December 23, 2014
Sunday, December 21, 2014
*** Mucosal immunization with an attenuated Salmonella vaccine partially protects white-tailed deer from chronic wasting disease
Tuesday, November 04, 2014
*** Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011

Sunday, December 28, 2014


Friday, December 5, 2014
*** SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide OIE
BSE TSE PRION AKA MAD COW DISEASE ? ‘’the silence was deafening’’ ...tss
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European
the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.
Sunday, December 14, 2014
*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report
Wednesday, December 24, 2014
National Scrapie Eradication Program November 2014 Monthly Report Fiscal Year 2015
Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014
Transmissible Spongiform Encephalopathy TSE Prion Disease have now been discovered in a wide verity of species across North America. typical C-BSE, atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine, typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98 Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD in cervid is slowly spreading without any stopping it in Canada and the USA and now has mutated into many different strains. Transmissible Mink Encephalopathy TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease have been silently mutating and spreading in different species in North America for decades. The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion Firewall, of which we now know without a doubt, that it was nothing but ink on paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of banned mad cow feed has been put out into commerce, never to return, as late as December of 2013, serious, serious breaches in the FDA mad cow feed ban have been documented. The 2004 enhanced BSE surveillance program was so flawed, that one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
The BSE surveillance and testing have also been proven to be flawed, and the GAO and OIG have both raised serious question as to just how flawed it has been (see GAO and OIG reports). North America has more documented TSE prion disease, in different documented species (excluding the Zoo BSE animals in the EU), then any other place on the Globe. This does not include the very likelihood that TSE prion disease in the domestic feline and canine have been exposed to high doses of the TSE prion disease vid pet food. To date, it’s still legal to include deer from cwd zone into pet food or deer food. Specified Risk Material i.e. SRM bans still being breach, as recently as just last month. nvCJD or what they now call vCJD, another case documented in Texas last month, with very little information being released to the public on about this case? with still the same line of thought from federal officials, ‘it can’t happen here’, so another vCJD blamed on travel of a foreign animal disease from another country, while ignoring all the BSE TSE Prion risk factors we have here in the USA and Canada, and the time that this victim and others, do spend in the USA, and exposed to these risk factors, apparently do not count in any way with regard to risk factor. a flawed process of risk assessment. sporadic CJD, along with new TSE prion disease in humans, of which the young are dying, of which long duration of illness from onset of symptoms to death have been documented, only to have a new name added to the pot of prion disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a familial type disease could be sporadic with no genetic link to any family member? when the USA is the only documented Country in the world to have documented two different cases of atypical H-type BSE, with one case being called atypical H-G BSE with the G meaning Genetic, with new science now showing that indeed atypical H-type BSE is very possible transmitted to cattle via oral transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada, USA, and the UK, with the same old excuse, better surveillance. You can only use that excuse for so many years, for so many decades, until one must conclude that CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a blip or a reason of better surveillance, it is a mathematical rise in numbers. More and more we are seeing more humans exposed in various circumstance in the Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same time in North America, more and more humans are becoming exposed to the TSE prion disease via consumption of the TSE prion via deer and elk, cattle, sheep and goats, and for those that are exposed via or consumption, go on to further expose many others via the iatrogenic modes of transmission of the TSE prion disease i.e. friendly fire. I pondered this mode of transmission via the victims of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone sub-clinical with sFFI or sGSS ? what if?
Two decades have passed since Dr. Ironside first confirmed his first ten nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is transmissible. yet all these TSE prion disease and victims in the USA and Canada are being pawned off as a spontaneous event, yet science has shown, the spontaneous theory has never been proven in any natural case of TSE prion disease, and scientist have warned, that they have now linked some sporadic CJD cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about this in the public domain. We must make all human and animal TSE prion disease reportable in every age group, in ever state and internationally, we must have a serious re-evaluation and testing of the USA cattle herds, and we must ban interstate movement of all cervids. Any voluntary effort to do any of this will fail. Folks, we have let the industry run science far too long with regards to the TSE prion disease. While the industry and their lobbyist continues to funnel junk science to our decision policy makers, Rome burns. ...end
Sunday, June 29, 2014
Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014
>>>There is no evidence that sporadic CJD is caused by what a person eats.<<<
2014 risk factors for sporadic cjd
***Moreover, L-BSE has been transmitted more easily to transgenic mice overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
***It has been suggested that some sporadic CJD subtypes in humans may result from an exposure to the L-BSE agent. Lending support to this hypothesis, pathological and biochemical similarities have been observed between L-BSE and an sCJD subtype (MV genotype at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and another sCJD subtype (MM genotype) [15].
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
*** Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2.
These data suggest that more than one BSEderived prion strain might infect humans;
***it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.
These studies further strengthen the evidence that vCJD is caused by a BSE-like prion strain.
Also, remarkably, the key neuropathological hallmark of vCJD, the presence of abundant florid PrP plaques, can be recapitulated on BSE or vCJD transmission to these mice.
***However, the most surprising aspect of the studies was the finding that an alternate pattern of disease can be induced in 129MM Tg35 mice from primary transmission of BSE, with a molecular phenotype indistinguishable from that of a subtype of sporadic CJD. This finding has important potential implications as it raises the possibility that some humans infected with BSE prions may develop a clinical disease indistinguishable from classical CJD associated with type 2 PrPSc. This is, in our experience, the commonest molecular sub-type of sporadic CJD. In this regard, it is of interest that the reported incidence of sporadic CJD has risen in the UK since the 1970s (Cousens et al., 1997)...
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.
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A"
To: "''"
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, ***yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.
Emmanuel Asante
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: (until 9/12/02) New e-mail: (active from now)
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far
*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
Tuesday, November 04, 2014
The pathological and molecular but not clinical phenotypes are maintained after second passage of experimental atypical bovine spongiform encephalopathy in cattle
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European
the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.
Sunday, December 14, 2014
ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report
Tuesday, November 04, 2014
Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease
Public Health implications
We have previously estimated a population-attributable proportion of surgically transmitted sCJD in Denmark and Sweden of 18%. This estimate was based mainly on surgery performed on middle-aged and elderly patients [6]. If susceptibility is age-related, as the present analysis indicate, the population-attributable fraction was underestimated. This idea is based on the fact that under-registration of SP prior to 1970 was highest for those first exposed at ages ,30 years, and that positive life-time surgical history in the UK at these ages reaches 60% [23]. Hence, risk of sCJD might be highest for ages at surgery not completely covered by our study. Estimating the public health impact would require a study update to be conducted after a 10-year interval, ie, at the present, to cover surgery at lower ages and infrequent, high-risk procedures such as neurosurgery.
Our results may imply that written recommendations for prevention, such as the need for single-use equipment, and for organizational measures may be particularly relevant for young surgical patients [24]. In addition, middle-aged and elderly patients inadvertently exposed to potentially contaminated instruments might not qualify as "at-risk persons for public health purposes", in view of their lower risk of acquiring sCJD. The results of this study would also support the need for EU Member States to implement continued surveillance of and public health research into all CJD forms, and the recording of patients’ complete surgical histories.
To sum up, the results of this study suggest that, in line with reported findings for iCJD and vCJD, there is an age-at-exposurerelated susceptibility for risk of sCJD from routine surgery. This observation is relevant for epidemiologic research, clinical guidance to prevent CJD transmission in medical settings, and CJD surveillance.
Tuesday, November 04, 2014
Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease
Wednesday, September 10, 2014
Creutzfeldt-Jakob disease (CJD) biannual update (August 2014), with updated guidance on decontamination of gastrointestinal endoscopy equipment
Research and analysis
Sunday, July 06, 2014
*** Dietary Risk Factors for Sporadic Creutzfeldt-Jakob Disease: A Confirmatory Case-Control Study Conclusions—The a priori hypotheses were supported.
***Consumption of various meat products may be one method of transmission of the infectious agent for sCJD.
***Results—Using control self-responses, consumption of hot dogs, sausage, pepperoni, kielbasa, “other” canned meat, poultry liver, any stomach/intestine, beef stomach/intestine, any organ tissue, and beef organ tissue was individually associated with increased sCJD risk; odds ratios (OR) ranged from 2.4 to 7.2 (0.003
*** Conclusions—The a priori hypotheses were supported. Consumption of various meat products may be one method of transmission of the infectious agent for sCJD.
Sunday, August 11, 2013
Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***
Tuesday, May 28, 2013
Late-in-life surgery associated with Creutzfeldt-Jakob disease: a methodological outline for evidence-based guidance
Saturday, November 16, 2013
Management of neurosurgical instruments and patients exposed to creutzfeldt-jakob disease 2013 December
Infect Control Hosp Epidemiol.
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease
Tuesday, March 5, 2013
Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)
FDA believes current regulation protects the public from BSE but reopens comment period due to new studies
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014
*** Singeltary comment ;
Sunday, December 7, 2014
Scientific update on the potential for transmissibility of non-prion protein misfolding diseases PRIONOIDS
just made a promise, never forget, never let them forget...
MOM DOD 12/14/97 confirmed hvCJD Heidenhain Variant Creutzfeldt Jakob Disease Case Report
Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'
DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114 McCullough Bldg. Galveston, Texas 77555-0785 FAX COVER SHEET DATE: 4-23-98 TO: Mr. Terry Singeltary @ ------- FROM: Gerald Campbell FAX: (409) 772-5315 PHONE: (409) 772-2881 Number of Pages (including cover sheet): Message: *CONFIDENTIALITY NOTICE* This document accompanying this transmission contains confidential information belonging to the sender that is legally privileged. This information is intended only for the use of the individual or entry names above. If you are not the intended recipient, you are hereby notified that any disclosure, copying distribution, or the taking of any action in reliances on the contents of this telefaxed information is strictly prohibited. If you received this telefax in error, please notify us by telephone immediately to arrange for return of the original documents.
Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q
Age: 63
YRS DOB: 10/17/34
Sex: F
Admitting Race: C
Attending Dr.: Date / Time Admitted : 12/14/97 1228
Copies to: UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
Autopsy' Office (409)772-2858 Autopsy NO.: AU-97-00435 AUTOPSY INFORMATION:
Occupation: Unknown Birthplace: Unknown Residence: Crystal Beach Date/Time of Death: 12/14/97 13:30 Date/Time of Autopsy: 12/15/97 15:00 Pathologist/Resident: Pencil/Fernandez Service: Private Restriction:
Brain only FINAL AUTOPSY DIAGNOSIS I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
snip...see full text ;
Saturday, December 13, 2014
Terry S. Singeltary Sr. Publications TSE prion disease
for my files...tss
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Time-Scaled Evolutionary Analysis of the Transmission and Antibiotic Resistance Dynamics of Staphylococcus aureus Clonal Complex 398
M. J. Warda, C. L. Gibbonsa, P. R. McAdamb, B. A. D. van Bunnika, E. K. Girvanc, G. F. Edwardsc, J. R. Fitzgeraldb and M. E. J. Woolhousea aCentre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh, United Kingdom bThe Roslin Institute and Edinburgh Infectious Diseases, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, United Kingdom cScottish MRSA Reference Laboratory, National Health Service Greater Glasgow and Clyde, Glasgow Royal Infirmary, Glasgow, United Kingdom C. A. Elkins, Editor + Author Affiliations
Next Section ABSTRACT Staphylococcus aureus clonal complex 398 (CC398) is associated with disease in humans and livestock, and its origins and transmission have generated considerable interest. We performed a time-scaled phylogenetic analysis of CC398, including sequenced isolates from the United Kingdom (Scotland), along with publicly available genomes. Using state-of-the-art methods for mapping traits onto phylogenies, we quantified transitions between host species to identify sink and source populations for CC398 and employed a novel approach to investigate the gain and loss of antibiotic resistance in CC398 over time. We identified distinct human- and livestock-associated CC398 clades and observed multiple transmissions of CC398 from livestock to humans and between countries, lending quantitative support to previous reports. Of note, we identified a subclade within the livestock-associated clade comprised of isolates from hospital environments and newborn babies, suggesting that livestock-associated CC398 is capable of onward transmission in hospitals. In addition, our analysis revealed significant differences in the dynamics of resistance to methicillin and tetracycline related to contrasting historical patterns of antibiotic usage between the livestock industry and human medicine. We also identified significant differences in patterns of gain and loss of different tetracycline resistance determinants, which we ascribe to epistatic interactions between the resistance genes and/or differences in the modes of inheritance of the resistance determinants.
In conclusion, we have performed a time-scaled phylogenetic analysis of CC398 and provided a quantitative understanding of the circulation of CC398 through separate human- and livestock-associated lineages, but with livestock also a significant source of human infection. We have also carried out a quantitative phylogenetic analysis of the loss and gain of antibiotic resistance determinants. However, human and livestock populations are linked in many ways, including agriculture, the food chain, and shared environments (39). In the future, further studies of a range of bacterial species and strains, using a large number of sequences from numerous potential sources of infection, are required to develop a more detailed understanding of the spread of bacteria and antibiotic resistance.
New Executive Actions to Combat Antibiotic Resistance and Protect Public Health Lisa Monaco, Dr. John P. Holdren September 18, 2014 02:33 PM EDT Today, the Obama administration is announcing a comprehensive set of new federal actions to combat the rise of antibiotic-resistant bacteria and protect public health. Additionally, the President’s Council of Advisors on Science and Technology (PCAST) is releasing a related report on Combating Antibiotic Resistance.
The discovery of antibiotics in the early 20th century fundamentally transformed medicine; antibiotics now save millions of lives each year in the United States and around the world. Yet bacteria repeatedly exposed to the same antibiotics can become resistant to even the most potent drugs. These so-called antibiotic-resistant bacteria can present a serious threat to public health, national security, and the economy.
In fact, according to the Centers for Disease Control and Prevention, antibiotic-resistant infections are associated with an additional 23,000 deaths and 2 million illnesses in the United States each year. The estimated annual impact of antibiotic-resistant infections on the national economy is $20 billion in excess direct health care costs, and as much as $35 billion in lost productivity from hospitalizations and sick days. Antibiotics are also critical to many modern medical interventions, including chemotherapy, surgery, dialysis, and organ transplantation.
The Administration is ramping up our efforts to combat antibiotic-resistant bacteria through a series of new actions including:
An Executive Order directing the federal government to work domestically and internationally to reduce the emergence and spread of antibiotic-resistant bacteria and to help ensure the continued availability of effective treatments for bacterial infections. The Executive Order establishes a new interagency Task Force and Federal Advisory Council and includes calls for better monitoring of resistant infections, improved regulations governing antibiotic use, more robust research to develop new and effective methods for combating antibiotic resistance, and increased international cooperation to curb the global rise in resistant bacteria. Importantly, the Executive Order directs the new interagency Task Force to develop a five-year National Action Plan for implementing both the National Strategy for Combating Antibiotic-Resistant Bacteria, which includes goals, milestones, and assessment metrics for detecting, preventing, and controlling antibiotic-resistant bacteria, and to address the new PCAST report. A National Strategy for Combating Antibiotic-Resistant Bacteria, which articulates national goals, priorities, and specific objectives that provide an overarching framework for federal investments aimed at combating antibiotic resistance. These include: preventing the spread of resistant bacteria; strengthening national efforts to identify instances of antibiotic resistance; working to develop new antibiotics, therapies, and vaccines; and improving international collaboration on this issue. A new PCAST report entitled Combating Antibiotic Resistance, containing recommendations that were developed by PCAST in consultation with a diverse group of experts that span the human and veterinary sectors for actions that the federal government can take to strengthen the nation’s ability to combat antibiotic-resistant bacteria. The launch of a $20 million prize sponsored by the National Institutes of Health, Biomedical Advanced Research and Development Authority, and the Food and Drug Administration to facilitate the development of a rapid diagnostic test to be used by health care providers to identify highly resistant bacterial infections at the point of patient care. These actions will help the nation contain the spread of resistant bacterial strains, manage existing antibiotics to prevent the development of new resistant strains, and help guarantee a steady pipeline of new, effective antibiotics and diagnostics. Most importantly, these actions will help save thousands of lives each year.
Learn more:
FACT SHEET: Obama Administration Takes Actions to Combat Antibiotic-Resistant Bacteria Lisa Monaco is Assistant to the President for Homeland Security & Counterterrorism. Dr. John P. Holdren is Assistant to the President for Science and Technology and Director of the White House Office of Science and Technology Policy.
BRAVO ! when you can’t fix stupid simply because of money, somebody has to do something... BRAVO !
Sunday, September 22, 2013
Livestock Origin for a Human Pandemic Clone of Community-Associated Methicillin-Resistant Staphylococcus aureus
Tuesday, September 17, 2013
Antibiotic resistance threats in the United States, 2013 THREAT REPORT
Thursday, September 18, 2014
New Executive Actions to Combat Antibiotic Resistance and Protect Public Health
*** Our investigation also found that you hold animals under conditions that are so inadequate that medicated animals bearing potentially harmful drug residues are likely to enter the food supply. For example, you failed to maintain complete treatment records. Food from animals held under such conditions is adulterated within the meaning of section 402(a)(4) of the FD&C Act, 21 U.S.C. § 342(a)(4).
Tuesday, September 17, 2013
Antibiotic resistance threats in the United States, 2013 THREAT REPORT
“We continue to promote the concept that, if an animal is sick, using antibiotics to treat that animal is obviously important,” said CDC Director Dr. Tom Frieden. “We also know that there are specific situations in which the widespread use of antimicrobials in agriculture has resulted in an increase in resistant infections in humans.”
just made a promise to mom, never forget, and never let them forget...
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas 77518