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
TSS
posted by Terry S. Singeltary Sr. at
10:37 AM
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