Tuesday, November 04, 2014

Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease

Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease

 

Jesu´ s de Pedro-Cuesta1*, Ignacio Mahillo-Fernandez1, Miguel Calero2, Alberto Ra´bano3, Mabel Cruz4, A° ke Siden4, Pablo Martı´nez-Martı´n1, Henning Laursen5, Marı´a Ruiz-Tovar1, Ka°re Mølbak6, on behalf of the EUROSURGYCJD Research Group"

 

1 Department of Applied Epidemiology, National Centre for Epidemiology, Carlos III Institute of Health; and Consortium for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Madrid, Spain, 2 Carlos III Institute of Health, and Consortium for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Majadahonda, Spain; and Alzheimer’s Disease Center, Reina Sofia Foundation, Madrid, Spain, 3 Alzheimer’s Disease Center, Reina Sofia Foundation, Madrid, Spain, 4 Karolinska Institute, Neurology Division, Stockholm, Sweden, 5 National Hospital, Copenhagen, Denmark, 6 Statens Serum Institut, Copenhagen, Denmark

 

Abstract

 

Introduction: Sporadic Creutzfeldt-Jakob disease (sCJD) might be transmitted by surgery. The purpose of this study was to investigate potential susceptibility to sCJD from surgery at juvenile age and in early adulthood.

 

Methods: From Danish and Swedish national registries we identified 167 definite and probable sCJD cases with onset from 1987 through 2003, and 835 age-, sex- and residence-matched controls along with their surgical histories. Main, anatomically or etiologically classified surgical procedures followed by a $20-year lag were analyzed using logistic regression, and stratified by age at first-registered surgical discharge.

 

Results: The risk of having a diagnosis of CJD depended strongly on age at first surgery with odds ratio (OR) of 12.80 (95% CI 2.56–64.0) in patients ,30 years, 3.04 (95% 1.26–7.33) in 30–39 years, and 1.75 (95% CI 0.89–3.45) in $40 years, for anatomically classified surgical procedures. Similar figures were obtained for etiologically classified surgical procedures.

 

Conclusions: Risk of surgical-acquired sCJD depends on age at exposure; this pattern is similar to age-specific profiles reported for CJD accidentally transmitted by human pituitary-derived growth hormone and susceptibility curves for variant CJD estimated after adjustment for dietary exposure to bovine spongiform encephalopathy. There might be an age-atexposure- related susceptibility to acquire all CJD forms, including sCJD from routine surgery.

 

SNIP...

 

Surgical history and risk of sCJD

 

A recent review of 18 case-control studies which examined links between medical procedures, particularly surgery and blood transfusion, and sCJD, identified many other associations, including protective ones, and highlighted diverse sources of potentially underlying bias [2]. The review concluded that potential methodological pitfalls in case-control studies on surgery and risk of sCJD were (a) the use of hospital controls and sampling controls close to or at the end of long case incidence periods, (b) exposure assessment in different lifetime periods for cases and controls and (c) potential confounding by concurrent procedures, particularly surgery and intra-operative blood transfusions. Three types of positive associations with decreasing biological plausibility were proposed. a) An increased frequency of surgery during the prodromal phase or early clinical course in sCJD was considered to be a stressful trigger of sCJD [22] or, alternatively, attributed to reverse causality by prodromal or subclinical disease [14]. b) Positive associations for SP and blood tranfusions, with the strongest evidence of an association based on latency analysis at .10- or .20-year lag, were consistent with the protracted incubation periods in human prion disease, but might have involved organs or tissues that are not known to be infectious in sCJD [9,10]. Although case-control studies must be interpreted with caution and there may be confounding of SP by BT, the positive findings in relation to SP and BT may indicate a true risk for sCJD c) As a third explanation, specific procedures at a shorter latency could be a risk factor, e.g. retinal surgery with about a mean 10-year lag or coronary surgery in the decade preceding sCJD onset. The interpretation of these findings required an assessment of specific, speculative hypotheses. Possibilities include the direct spread of prions to the retina, or the confounding by risk factors shared by coronary disease and sCJD [6,14]. For details we refer the reader to our abovementioned review.

 

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.

 

Figure 1. Potential age-at-exposure-related susceptibility for the following different CJD forms and exposures: (a) Age-susceptibility function for vCJD in the UK [12], and results from Table 1 for risk of sCJD from age at first hospital discharge associated with a registered, main surgical procedure, at a lag of $20 years. (b) Reported estimated risks relating to 5- to 10-year age groups, after adjustment for dietary exposure to bovine material and average incubation period established at 12.6 years for variant CJD in the UK [13], and plotted results from Table 1 for risk of sCJD from age at first hospital discharge associated with an etiologically reclassified higher-risk or lower-risk procedure, at a lag of $20 years. (c) Reported rate ratios of accidentally transmitted CJD (iCJD), for ever treatement vs never treatement with pituitary growth hormone (all treatments) at specific ages [11]. Reference: all other ages at treatment. (d) Reported rate ratios of accidentally transmitted CJD (iCJD) for ever treatment vs never treatment with pituitary growth hormone processed with the Hartree-modified Wilhelmi method (an hGH preparation associated with highest risk of iCJD among hGH-treated cohorts) at specific ages [11]. Reference: all other ages at treatment.

 

Citation: de Pedro-Cuesta J, Mahillo-Fernandez I, Calero M, Ra´bano A, Cruz M, et al. (2014) Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease. PLoS ONE 9(10): e109412. doi:10.1371/journal.pone.0109412

 

Editor: Noriyuki Nishida, Nagasaki University Graduate School of Biomedical Sciences, Japan

 

Received June 11, 2014; Accepted August 30, 2014; Published October 3, 2014

 

Copyright: 2014 de Pedro-Cuesta et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Data Availability: The authors confirm that all data underlying the findings are fully available without restriction. The data contains detailed information on treatment in hospitals at the individual level and it is unsuitable for public deposition. The data are available upon request to all interested researchers, and requests should be submitted to: Dr. Ka°re Mølbak (Epidemiology Department, Statens Serum Institute, Copenhagen, Denmark , KRM@ssi.dk, Artilleriva¨gen).

 

Funding: Funding was obtained from the EU Research Commission, Concerted Action QLRG3-CT-2002-81223, NEUROPRION and the Spanish Centro de Investigaciones en enfermedades Neurolo´ gicas (CIEN C03-06), and Consortium for Biomedical Research in Neurodegenerative Diseases (CIBERNED) networks, and from the Karolinska and Carlos III National Health Institutes. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 

Competing Interests: The authors have declared that no competing interests exist.

 

* Email: jpedro@isciii.es

 

" Membership of the EUROSURGYCJD Research Group is provided in the Acknowledgments.

 

 

doi:10.1371/journal.pone.0109412.g001 Age-Dependent Induction of Acquired and Sporadic CJD PLOS ONE | www.plosone.org 5 October 2014 | Volume 9 | Issue 10 | e109412

 

SEE FULL TEXT ;

 


 

ONCE AGAIN, MANY THANKS TO PLOS ET AL FOR FULL TEXT ACCESS TO THE LAY PUBLIC...TSS

 

Monday, November 3, 2014

 

The prion protein protease sensitivity, stability and seeding activity in variably protease sensitive prionopathy brain tissue suggests molecular overlaps with sporadic Creutzfeldt-Jakob disease

 


 


 

Friday, January 10, 2014

 

*** vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???  ***

 


 

Monday, November 3, 2014

 

USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014

 

National Prion Disease Pathology Surveillance Center Cases Examined1 (October 7, 2014)

 

***6 Includes 11 cases in which the diagnosis is pending, and 19 inconclusive cases; ***7 Includes 12 (11 from 2014) cases with type determination pending in which the diagnosis of vCJD has been excluded. ***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob disease (sCJD),

 

***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)

 

***and 21 cases of sporadic Fatal Insomnia (sFI).

 


 

Sunday, April 06, 2014

 

SPORADIC CJD and the potential for zoonotic transmission there from, either directly or indirectly via friendly fire iatrogenic mode, evidence to date

 


 

Tuesday, February 11, 2014

 

Novant Health Forsyth Medical Center Information on potential CJD exposure

 


 

 

Tuesday, April 01, 2014

 

Questions linger in U.S. CJD cases 2005, and still do in 2014

 


 

Sunday, March 09, 2014

 

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

 

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES

 


 

Friday, February 14, 2014

 

Creutzfeldt-Jakob disease (CJD) biannual update (February 2014), with briefing on novel human prion disease National CJD Research and Surveillance Unit NCJDRSU

 


 

Thursday, April 17, 2014

 

Novant: Three more may have been exposed to disease CJD

 


 

Wednesday, April 02, 2014

 

Distinct origins of dura mater graft-associated Creutzfeldt-Jakob disease: past and future problems

 


 

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 ***

 


 

Sunday, October 13, 2013

 

*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012

 


 

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.

 


 

Sunday, June 29, 2014

 

*** Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014

 


 

Wednesday, February 26, 2014

 

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION 2004 THROUGHT PRION 2013 CONFERENCE ABSTRACT BOOKS

 


 

Thursday, January 23, 2014

 

Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) [Docket No. FDA–2013–D–1574]

 


 

Letters

 

JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

Terry S. Singeltary, Sr Bacliff, Tex

 

Since this article does not have an abstract, we have provided the first 150 words of the full text.

 

KEYWORDS: creutzfeldt-jakob disease, diagnosis. To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

 

References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.

 


 

14th ICID International Scientific Exchange Brochure - Final Abstract Number: ISE.114

 

Session: International Scientific Exchange

 

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

 

T. Singeltary Bacliff, TX, USA

 

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

 

Methods: 12 years independent research of available data

 

Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

 

Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

 


 

 Wednesday, May 16, 2012

 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

Background

 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.

 

Methods

 

Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.

 

Results

 

I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.

 

Conclusions

 

There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.

 

end...tss

 

SEE FULL TEXT AND SOURCE REFERENCES ;

 

Wednesday, May 16, 2012

 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

Proposal ID: 29403 ‘ACCEPTED’

 


 

The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI

 

Tracking spongiform encephalopathies in North America

 

Original

 

Xavier Bosch

 

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...

 


 


 

SEE FULL TEXT ;

 

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

 

Subject: Tracking spongiform encephalopathies in North America LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003

 

Date: Tue, 29 Jul 2003 17:35:30 –0500

 

From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy

 

To: BSE-L@uni-karlsruhe.de

 

Volume 3, Number 8 01 August 2003

 

Previous

 

Next

 

Newsdesk

 

Tracking spongiform encephalopathies in North America

 

Xavier Bosch

 

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

 

49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.

 

Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.

 

Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.

 

To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.

 

Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.

 

Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.

 

Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.

 

Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.

 

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.

 

CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.

 


 

Singeltary submission to PLOS ;

 

No competing interests declared.

 

see full text ;

 


 

Re: vCJD in the USA * BSE in U.S. 15 November 1999 Terry S Singeltary, NA

 

CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997. So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie.

 

It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses.

 


 

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... 2 January 2000 Terry S Singeltary

 

The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;

 

"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."

 

Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.

 

Something else I find odd, page 16;

 

"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."

 

A few more factors to consider, page 15;

 

"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."

 

"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."

 

"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."

 

Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.

 

To be continued...

 

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

 

Competing interests: None declared

 


 

Singeltary Response to USDA, and USDA RESPONSE TO SINGELTARY ON HARVARD BSE RISK ASSESSMENT

 

Owens, Julie

 

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

 

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

 


 

FSIS, USDA, REPLY TO SINGELTARY

 


 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

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

 

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

 

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

 

PRODUCT

 

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

 

CODE

 

Cattle feed delivered between 01/12/2007 and 01/26/2007

 

RECALLING FIRM/MANUFACTURER

 

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

 

Firm initiated recall is ongoing.

 

REASON

 

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

 

VOLUME OF PRODUCT IN COMMERCE

 

42,090 lbs.

 

DISTRIBUTION

 

WI

 

___________________________________

 

PRODUCT

 

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

 

CODE

 

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

 

RECALLING FIRM/MANUFACTURER

 

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

 

REASON

 

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

 

VOLUME OF PRODUCT IN COMMERCE

 

9,997,976 lbs.

 

DISTRIBUTION

 

ID and NV

 

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

 


 

Sunday, December 15, 2013

 

*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE ***

 


 

Tuesday, August 12, 2014

 

MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST 2014

 


 

Thursday, June 23, 2011

 

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits

 


 

Wednesday, April 25, 2012 4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012

 


 

2012 ATYPICAL L-TYPE BSE BASE CALIFORNIA ‘confirmed’ Saturday, August 4, 2012

 

*** Final Feed Investigation Summary - California BSE Case - July 2012

 


 

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