2/3/2008
covering up mad cow disease?
From Pat Dollard.
I had previously put up a post about waterboarding cows, tongue-in-cheek.
The video shows it’s a serious and frightening thing.
Schools scramble to find questionable meat-LA Times:
The California Department of Education on Thursday urged all schools in the state to temporarily strike from the menu any item containing ground beef, as the U.S. Department of Agriculture investigated claims that Hallmark Meat Packing butchered so-called downer cattle that are too weak to walk.
A video released Wednesday by the Humane Society of the United States showed workers at Hallmark dragging downed animals by their legs or using forklifts and water hoses to force weak cattle to their feet, prompting the federal investigation.
The USDA banned “non-ambulatory” cattle from the human food supply last year because inability to walk may be a sign of bovine spongiform encephalopathy, commonly known as mad cow disease. Studies in Europe found that cattle that were unable to rise or walk were more likely than other cattle to carry the disease, which can be transferred to humans through consumption.
Just last year ‘non-ambulatory’ cattle were banned from the human food supply? What about the animal food supply? How long has this been going on before the ban?
My family has been talking about this silent epidemic for some time. I wonder if it will slip back under the covers.
Articles:
First apparent U.S. case of mad cow disease discovered-CNN, 2003
February 5th, 2008 at 6:17 pm
for Pete’s sake, that’s insane !!!
i have wasted a decade daily researching this, and ever bit of
this suspect product or any product from this company should be pulled from
the shelf NOW. DOWNERS are highly suspect BSE, and in the USA, the last two
documented mad cows were of the atypical h-BASE BSE mad cow strain i.e.
bovine spongiform encephalopathy, this strain is MORE VIRULENT TO HUMANS
than the UK BSE strain. please read the science and sources
below……………….terry
THE SPIN ;
Release No. 0028.08
Contact:
Office of Communications (202) 720-4623
TRANSCRIPT: USDA Officials Hold Technical Briefing Regarding Inhumane
Handling Allegations
Washington January 31, 2008
snip…
http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2008/02/0028.xml
THE FACTS ;
> TRANSCRIPT: USDA Officials Hold Technical Briefing Regarding Inhumane
> Handling Allegations
THE title is very misleading. A better title in my opinion would have read ;
HIGHLY SUSPECT BSE, H-BASE, MAD COW BEEF DISTRIBUTED NATIONALLY (35 states
to date), to CHILDREN AND THE ELDERLY
USDA CERTIFIED H-BASE MAD COW SCHOOL LUNCH PROGRAM
http://cjdmadcowbaseoct2007.blogspot.com/2008/02/usda-certified-h-base-mad-cow-school.html
It’s the American way $$$
PRION DISEASE UPDATE 2008 (03)
******************************
A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases
[With the continuing decline of the number of cases of variant
Creutzfeldt-Jacob disease (abbreviated previously as vCJD or CJD (new
var.) in ProMED-mail) in the human population, it has been decided to
broaden the scope of the occasional ProMED mail reports to include
other prion-related diseases. Data on vCJD cases from any part of the
world are now included in these updates where appropriate, and other
forms of CJD (sporadic, iatrogenic, familial, and GSS
(Gerstmann-Straussler-Scheinker disease) are included also when they
have some relevance to the incidence and etiology of vCJD. - Mod.CP]
In this update:
[1] UK: National CJD Surveillance Unit — monthly statistics
[2] UK: SEAC 99th meeting report
[3] BASE transmission risk
******
[1] UK: National CJD Surveillance Unit — monthly statistics
Date: Fri 1 Feb 2008
Source: UK National CJD Surveillance Unit, monthly statistics [edited]
Monthly Creutzfeldt-Jakob disease statistics — as of 1 Feb 2008
—————————————————————-
These following figures show the number of suspect cases of CJD
referred to the CJD surveillance unit in Edinburgh and the number of
deaths of definite and probable variant Creutzfeldt-Jakob disease
[abbreviated in ProMED-mail as CJD (new var.) or vCJD], the form of
the disease thought to be linked to BSE (bovine spongiform
encephalopathy).
Definite and probable vCJD cases in the UK as of 1 Feb 2008
———————————————————–
Summary of vCJD cases — deaths
——————————————-
Deaths from definite vCJD (confirmed): 114
Deaths from probable vCJD (without neuropathological confirmation): 48
Deaths from probable vCJD (neuropathological confirmation pending): 1
Number of deaths from definite or probable vCJD (as above): 163
Summary of vCJD cases — alive
——————————
Number of probable vCJD cases still alive: 3
Total
—–
Number of definite or probable vCJD (dead and alive): 166
These data indicate that there have been no new cases diagnosed
during the past month, and the number of patients alive is unchanged.
These data are still consistent with the view that the vCJD outbreak
in the UK is in decline (although the incidence curve may be
developing a tail). The peak number of deaths was 28 in the year
2000, followed by 20 in 2001, 17 in 2002, 18 in 2003, 9 in 2004, 5 in
2005, 5 in 2006, 5 in 2007, and so far none in 2008
Totals for all types of CJD cases in the year 2008
————————————————–
As of 1 Feb 2008 in the UK in the year 2008 so far there have been 9
referrals, 6 deaths from sporadic CJD, one death from iatrogenic CJD,
none from familial CJD, none from GSS, and none from vCJD.
–
Communicated by:
ProMED-mail
******
[2] UK: SEAC 99th meeting report
Date: Thu 31 Jan 2008R (SEAC)
Source: Spongiform Encephalopathy Advisory Committee (SEAC), 99th
meeting, 14 Dec 2007 [edited]
READ FULL TEXT HERE…TSS
Update on vCJD and sCJD epidemiology
————————————
Dr Richard Knight (NCJDSU-National CJD Surveillance Unit) presented
an update on the epidemiology of cases of sporadic CJD (sCJD) and
vCJD in the UK and elsewhere. Between May 1990 and October 2007, 944
cases of sCJD had been identified in the UK with a mean age at onset
of 66 (range 15-94) years and mean age of death of 67 (range 20-95)
years. There is no significant gender difference in sCJD incidence.
There had been a trend towards an increasing number of cases over
time to almost 80 cases per year in 2003; this increased trend had
also been observed in other countries and was considered to be a
result of better surveillance and diagnosis of disease. There has
been a decline in number since 2003, but this may not be of
significance. The post mortem rate for sCJD referral is about 60
percent. The genotype distribution of sCJD cases was 64 percent MM,
18 percent MV and 18 percent VV at codon 129 of the prion protein
gene.
Dr Knight explained that the total number of definite and probable
vCJD cases in the UK up to November 2007 was 166, with 4 cases still
alive. 3 out of 4 vCJD cases treated with pentosan polysulphate (PPS)
had appreciably longer survival times, but it is not proven that this
is the result of treatment. No statistically significant gender
difference had been observed in vCJD cases. The age distribution of
vCJD had not altered over the course of the UK epidemic, with the
median age of death of 30 (range 14-75) years. Statistical analysis
of the UK incidence of deaths from vCJD suggested the epidemic had
peaked in 2000 with 28 deaths. There are 3 cases identified with
onset in 2006 and four deaths in 2007. Geographical distribution of
vCJD cases in the UK shows higher incidence in the North than South.
All 146 vCJD cases tested to date are of the MM genotype [but see
ProMED-mail Prion disease update 2008 (02) 20080107.0087 for a recent
exception. - Mod.CP]
Dr Knight explained that elsewhere in the world up to November 2007,
39 vCJD cases have been reported with 23 in France, 4 in the Republic
of Ireland (RoI), 3 in the USA, 2 in the Netherlands, 2 in Portugal
and single cases in Italy, Canada, Japan, Saudi Arabia, and Spain.
Infection is considered likely to have occurred in the UK in 2 Ireland
cases, 2 USA cases, and the single French, Japanese & Canadian cases.
One of the French cases had a history of possibly significant
residence in the UK. One USA case is thought likely to have been
exposed to infection in Saudi Arabia, rather than the USA.
Dr Knight explained that the Transfusion Medicine Epidemiology Review
study had identified 4 instances of vCJD infection resulting from
receipt of non-leucodepleted [white cell reduced] red blood cells
donated by individuals who had subsequently developed vCJD. The donors
developed clinical vCJD ranging from 17 months to 3.5 years after
blood donation and this indicates that blood can be infective 3.5
years before the development of clinical disease. Clinical vCJD was
identified in 3 recipients (all of MM genotype) between 6.5 and 8.3
years after receipt of blood. The 4th recipient, who died of
non-neurological disease, with only lymphoreticular evidence of vCJD
infection, was of MV genotype.
In response to a question about the neuropathology of the vCJD case
that died after receiving PPS, Dr Knight explained that no autopsy
was undertaken.
A member asked about the reason for the increase in sCJD detection in
the years up to 2003. Dr Knight replied that it was probably due to
better awareness of the disease and the availability of better
diagnostic methods such as cerebrospinal fluid testing and magnetic
resonance imaging.
Mr Mark Noterman (Department of Health [DH]) asked whether the
neuropathological referrals rate had increased after the Chief
Medical Officer’s letter to clinicians earlier in the year to remain
vigilant about cases of neurological disease that could be related to
prion disease. Dr Knight replied that there had been no subsequent
significant increase in referral rate.
–
Communicated by:
Terry S. Singeltary Sr.
******
[3] BASE transmission risk
Date: Wed 30 Jan 2008
Source: Journal of Virology, Wed 20 Jan 2008 [edited]
Evaluation of the human transmission risk of an atypical bovine
spongiform encephalopathy prion strain
—————————————————————
The following is the Abstract of a paper published in the Journal of
Virology by Qingzhong Kong and colleagues at the Department of
Pathology, Case Western Reserve University, Cleveland, Ohio 44106,
USA; CEA [Centro di Referenza per le Encefalopatie Animali], and the
Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy;
Department of Neurological and Visual Sciences, University of Verona,
37134 Verona, Italy.
“Bovine spongiform encephalopathy (BSE), the prion disease in cattle,
was widely believed to have only one strain (BSE-C). BSE-C causes the
fatal prion disease named new variant Creutzfeldt-Jacob [vCJD]
disease in humans. Since 2004, 2 atypical BSE strains, BASE [bovine
amyloidotic spongiform encephalopathy] (or BSE-L) and BSE-H, have
been discovered in several countries ; their transmissibility and
phenotypes in humans are unknown. We investigated the infectivity and
human phenotype of BASE by inoculating transgenic (Tg) mice
expressing the human prion protein with brain homogenates from 2
BASE-affected cattle. 60 percent of the inoculated Tg mice became
infected after 20-22 months incubation, a transmission rate higher
than those reported for BSE-C. A quarter of BASE-infected Tg mice,
but none of the Tg mice infected with a sporadic human prion disease,
showed presence of pathogenic prion protein isoforms in the spleen,
indicating that the BASE prion is intrinsically lymphotropic. The
pathological prion protein isoforms in BASE-infected humanized Tg
mouse brains are different from those of the original cattle BASE or
sporadic human prion disease. Minimal brain spongiosis and long
incubation time are observed in the BASE-infected Tg mice. These
results suggest that, in humans, BASE is a more virulent BSE strain
and likely lymphotropic.”
–
Communicated by:
Terry S. Singeltary Sr.
[see also:
Prion disease update 2008 (02) 20080107.0087
Prion disease update 2008 (01): correction 20080104.0046
Prion disease update 2008 (01) 20080102.0014
2007
—-
Prion disease update 2007 (08) 20071205.3923
Prion disease update 2007 (07) 20071105.3602
Prion disease update 2007 (06) 20071003.3269
Prion disease update 2007 (05) 20070901.2879
Prion disease update 2007 (04) 20070806.2560
Prion disease update 2007 (03) 20070702.2112
Prion disease update 2007 (02) 20070604.1812
Prion disease update 2007 20070514.1542
CJD (new var.) update 2007 (05) 20070403.1130
CJD (new var.) update 2007 (04) 20070305.0780
CJD (new var.) update 2007 (03) 20070205.0455
CJD (new var.) update 2007 (02): South Korea, susp 20070115.0199
2006
—-
CJD (new var.), blood transfusion risk 20061208.3468
CJD, transmission risk - Canada (ON) 20061207.3457
CJD (new var.) update 2006 (12) 20061205.3431
CJD (new var.) update 2006 (11) 20061106.3190
CJD (new var.) update 2006 (10) 20061002.2820
CJD (new var.) - Netherlands: 2nd case 20060623.1741
CJD (new var.) - UK: 3rd transfusion-related case 20060209.0432
CJD (new var.) update 2006 (02) 20060206.0386
CJD (new var.) update 2006 20060111.0101
2005
—-
CJD (new var.) update 2005 (12) 20051209.3547
CJD (new var.) update 2005 (11) 20051108.3270
CJD (new var.) update 2005 (10) 20051006.2916
CJD (new var.) update 2005 (02) 20050211.0467
CJD (new var.) - UK: update 2005 (01) 20050111.0095
2004
—-
CJD, genetic susceptibility 20041112.3064
CJD (new var.) - UK: update 2004 (14) 20041206.3242
CJD (new var.) - UK: update 2004 (10) 20040909.2518
CJD (new var.) - UK: update 2004 (02) 20040202.0400
CJD (new var.) - UK: update 2004 (01) 20040106.0064
CJD (new var.) - France: 8th case 20041022.2864
CJD (new var.) - France: 9th case 20041123.3138
CJD (new var.), blood supply - UK 20040318.0758
CJD (new var.), carrier frequency study - UK 20040521.1365
2003
—-
CJD (new var.) - UK: update 2003 (13) 20031216.3072
CJD (new var.) - UK: update 2003 (01) 20030108.0057
2002
—-
CJD (new var.) - UK: update Dec 2002 20021207.5997
CJD (new var.) - UK: update Jan 2002 20020111.3223
2001
—-
CJD (new var.), incidence & trends - UK (02) 20011124.2875
CJD (new var.), incidence & trends - UK 20011115.2816
CJD (new var.) - UK: reassessment 20011029.2671
CJD (new var.) - UK: update Oct 2001 20011005.2419
CJD (new var.) - UK: regional variation (02) 20010907.2145
CJD (new var.) - UK: update Sep 2001 20010906.2134
CJD (new var.) - UK: update Aug 2001 20010808.1872
CJD (new var.) - UK: 9th Annual Report 20010628.1231
CJD (new var.) - UK: update June 2001 20010622.1188
CJD (new var.) - UK: update 3 Jan 2001 20010104.0025]
………………………………….cp/mj/jw
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Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734.
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Since this article does not have an abstract, we have provided the first 150
words of the full text and any section headings.
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.
Terry S. Singeltary, Sr
Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL
TEXT
http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
TSS
February 5th, 2008 at 6:18 pm
I would kindly like to reply about this suspect beef recall. suspect being
that any cow in that condition is suspect TSE i.e. BSE/BASE mad cow or
rabies. i have wasted over a decade daily investigating this issue. i can
assure you do not know all of what is going on. i wish to send this data to
you below. ………
p.s. this nightmare goes much further than the ukbsenvcjd hamburger eating
adolescents only theory.
Pandora’s box has been opened for some time, and friendly fire i.e. medical
and surgical arena will
play a huge role in spreading and exposing this agent to millions. …tss
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk
Materials for Human Food and Requirement for the Disposition of
Non-Ambulatory Disabled Cattle
03-025IFA
03-025IFA-2
Terry S. Singeltary
Page 1 of 17
9/13/2005
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
Audit Report
Animal and Plant Health Inspection Service
Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II
and
Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat
Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle
Still Remain
Our prior report identified a number of inherent problems in identifying and
testing high-risk cattle. We reported that the challenges in identifying the
universe of high-risk cattle, as well as the need to design procedures to
obtain an appropriate representation of samples, was critical to the success
of the BSE surveillance program. The surveillance program was designed to
target nonambulatory cattle, cattle showing signs of CNS disease (including
cattle testing negative for rabies), cattle showing signs not inconsistent
with BSE, and dead cattle. Although APHIS designed procedures to ensure FSIS
condemned cattle were sampled and made a concerted effort for outreach to
obtain targeted samples, industry practices not considered in the design of
the surveillance program reduced assurance that targeted animals were tested
for BSE.
In our prior report, we recommended that APHIS work with public health and
State diagnostic laboratories to develop and test rabies-negative samples
for BSE. This target group is important for determining the prevalence of
BSE in the United States because rabies cases exhibit clinical signs not
inconsistent with BSE; a negative rabies test means the cause of the
clinical signs has not been diagnosed.
APHIS agreed with our recommendation and initiated an outreach program with
the American Association of Veterinary Laboratory Diagnosticians, as well as
State laboratories. APHIS also agreed to do ongoing monitoring to ensure
samples were obtained from this target population.
Although APHIS increased the samples tested from this target group as
compared to prior years, we found that conflicting APHIS instructions on the
ages of cattle to test resulted in inconsistencies in what samples were
submitted for BSE testing. Therefore, some laboratories did not refer their
rabies negative samples to APHIS in order to maximize the number tested for
this critical target population. In addition, APHIS did not monitor the
number of submissions of rabies negative samples for BSE testing from
specific laboratories.
snip…
An NVSL official stated that APHIS is not concerned with rabies negatives
samples from cattle less than 30 months of age. This position, however, is
contrary to APHIS’ published target population.
Our prior audit recognized the significant challenge for APHIS to obtain
samples from some high-risk populations because of the inherent problems
with obtaining voluntary compliance and transporting the carcasses for
testing. USDA issued rules to prohibit nonambulatory animals (downers) from
entering the food supply at inspected slaughterhouses. OIG recommended, and
the International Review Subcommittee33 emphasized, that USDA should take
additional steps to assure that facilitated pathways exist for dead and
nonambulatory cattle to allow for the collection of samples and proper
disposal of carcasses. Between June 1, 2004, and May 31, 2005, the APHIS
database documents 27,617 samples were collected showing a reason for
submission of nonambulatory and 325,225 samples were collected with reason
of submission showing “dead.”
APHIS made extensive outreach efforts to notify producers and private
veterinarians of the need to submit and have tested animals from these
target groups. They also entered into financial arrangements with 123
renderers and other collection sites to reimburse them for costs associated
with storing, transporting, and collecting samples. However, as shown in
exhibit F, APHIS was not always successful in establishing agreements with
non-slaughter collection sites in some States. APHIS stated that agreements
do not necessarily reflect the entire universe of collection sites and that
the presentation in exhibit F was incomplete because there were many
collection sites without a payment involved or without a formal agreement.
We note that over 90 percent of the samples collected were obtained from the
123 collection sites with agreements and; therefore, we believe agreements
offer the best source to increase targeted samples in underrepresented
areas.
We found that APHIS did not consider industry practices in the design of its
surveillance effort to provide reasonable assurance that cattle exhibiting
possible clinical signs consistent with BSE were tested. Slaughter
facilities do not always accept all cattle arriving for slaughter because of
their business requirements. We found that, in one State visited, slaughter
facilities pre-screened and rejected cattle (sick/down/dead/others not
meeting business
Downers and Cattle that Died on the Farm standards) before presentation for
slaughter in areas immediately adjacent or contiguous to the official
slaughter establishment. These animals were not inspected and/or observed by
either FSIS or APHIS officials located at the slaughter facilities.
FSIS procedures state that they have no authority to inspect cattle not
presented for slaughter. Further, APHIS officials stated they did not
believe that they had the authority to go into these sorting and/or
screening areas and require that the rejected animals be provided to APHIS
for BSE sampling. Neither APHIS nor FSIS had any process to assure that
animals left on transport vehicles and/or rejected for slaughter arrived at
a collection site for BSE testing. FSIS allows slaughter facilities to
designate the area of their establishment where federal inspection is
performed; this is designated as the official slaughter establishment.34
We observed animals that were down or dead in pens outside the official
premises that were to be picked up by renderers. Animals that were rejected
by plant personnel were transported off the premises on the same vehicles
that brought them to the plant.35
A policy statement36 regarding BSE sampling of condemned cattle at slaughter
plants provided that effective June 1, 2004, FSIS would collect BSE samples
for testing: 1) from all cattle regardless of age condemned by FSIS upon
ante mortem inspection for CNS impairment, and 2) from all cattle, with the
exception of veal calves, condemned by FSIS upon ante mortem inspection for
any other reason.
FSIS Notice 28-04, dated May 20, 2004, informed FSIS personnel that, “FSIS
will be collecting brain samples from cattle at federally-inspected
establishments for the purpose of BSE testing.” The notice further states
that, “Cattle off-loaded from the transport vehicle onto the premises of the
federally-inspected establishment (emphasis added), whether dead or alive,
will be sampled by the FSIS Public Health Veterinarian (PHV) for BSE after
the cattle have been condemned during ante mortem inspection. In addition,
cattle passing ante mortem inspection but later found dead prior to
slaughter will be condemned and be sampled by the FSIS PHV.”
APHIS has the responsibility for sampling dead cattle off-loaded onto
plant-owned property that is adjoining to, but not considered part of, the
“official premises.37 FSIS procedures38 provide that “Dead cattle that are
off-loaded to facilitate the off-loading of live animals, but that will be
re-loaded onto the transport vehicle, are not subject to sampling by FSIS.
While performing our review in one State, we reviewed the circumstances at
two slaughter facilities in the State that inspected and rejected unsuitable
cattle before the animals entered the official receiving areas of the
plants. This pre-screening activity was conducted in areas not designated by
the facility as official premises of the establishment and not under the
review or supervision of FSIS inspectors. The plant rejected all
nonambulatory and dead/dying/sick animals delivered to the establishment.
Plant personnel refused to offload any dead or downer animals to facilitate
the offloading of ambulatory animals. Plant personnel said that the driver
was responsible for ensuring nonambulatory animals were humanely euthanized
and disposing of the carcasses of the dead animals. Plant personnel informed
us that they did not want to jeopardize contracts with business partners by
allowing unsuitable animals on their slaughter premises.
In the second case, one family member owned a slaughter facility while
another operated a livestock sale barn adjacent to the slaughter facility.
The slaughter facility was under FSIS’ supervision while the sale barn was
not. Cattle sometimes arrived at the sale barn that were sick/down/dead or
would die or go down while at the sale barn. According to personnel at the
sale barn, these animals were left for the renderer to collect. The healthy
ambulatory animals that remained were marketed to many buyers including the
adjacent slaughter facility. When the slaughter facility was ready to accept
the ambulatory animals for processing, the cattle would be moved from the
sale barn to the slaughter facility where they were subject to FSIS’
inspection.
We requested the slaughter facilities to estimate the number of cattle
rejected on a daily basis (there were no records to confirm the estimates).
We visited a renderer in the area and found that the renderer had a contract
with APHIS to collect samples for BSE testing. In this case, although we
could not obtain assurance that all rejected cattle were sampled, the
renderer processed a significant number of animals, as compared to the
slaughter plants’ estimates of those rejected. Due to the close proximity
(less than 5 miles) of the renderer to the slaughter facilities, and the
premium it paid for dead cattle that were in good condition, there was a
financial incentive for transport drivers to dispose of their dead animals
at this renderer.
USDA/OIG-A/50601-10-KC Page 25
In our discussions with APHIS officials in Wisconsin and Iowa, they
confirmed that there were plants in their States that also used
pre-screening practices. On May 27, 2005, we requested APHIS and FSIS to
provide a list of all slaughter facilities that pre-screened cattle for
slaughter in locations away from the area designated as the official
slaughter facility. Along with this request, we asked for information to
demonstrate that either APHIS or FSIS confirmed there was a high likelihood
that high-risk animals were sampled at other collection sites.
In response to our request, the APHIS BSE Program Manager stated that APHIS
did not have information on slaughter plants that pre-screen or screen their
animals for slaughter suitability off their official plant premises. To
their knowledge, every company or producer that submits animals for
slaughter pre-sorts or screens them for suitability at various locations
away from the slaughter facility. For this reason, USDA focused its BSE
sample collection efforts at other types of facilities such as renderers,
pet food companies, landfills, and dead stock haulers. Further, in a letter
to OIG on June 14, 2005, the administrators of APHIS and FSIS noted the
following:
“…we believe that no specific actions are necessary or appropriate to obtain
reasonable assurance that animals not presented for slaughter are being
tested for BSE. There are several reasons for our position. First, we do not
believe that the practice is in fact causing us to not test a significant
enough number of animals in our enhanced surveillance program to invalidate
the overall results. Second, OIG has concluded that because of the
geographical proximity and business relationships of the various entities
involved in the case investigated, there is reasonable assurance that a
majority of the rejected cattle had been sampled. Third, it is also
important to remember that the goal of the enhanced surveillance program is
to test a sufficient number of animals to allow us to draw conclusions about
the level of BSE (if any) in the American herd…We believe that the number we
may be not testing because of the “pre-sorting” practice does not rise to a
significant level. The number of animals tested to date has far exceeded
expectations, so it is reasonable to infer that there are few of the animals
in question, or that we are testing them at some other point in the
process…APHIS estimated…there were approximately 446,000 high risk
cattle…[and APHIS has]…tested over 375,000 animals in less than 1 year. This
indicated that we are missing few animals in the high-risk population,
including those that might be pre-sorted before entering a slaughter
facility’s property.”
snip…
APHIS notes that for the current surveillance program, it had established
regional goals and APHIS was not trying to meet particular sampling levels
in particular States. However, we believe that it would be advantageous for
APHIS to monitor collection data and increase outreach when large
geographical areas such as the above States do not provide samples in
proportion to the numbers and types of cattle in the population.
We also disagree with APHIS/FSIS’ contention that because they have tested
over 375,000 of their 446,000 estimate of high risk cattle, few in the
high-risk population are being missed, including those that might be
pre-screened before entering a slaughter facility’s property. In our prior
audit, we reported that APHIS underestimated the high-risk population; we
found that this estimate should have been closer to 1 million animals (see
Finding 1). We recognize that BSE samples are provided on a voluntary basis;
however, APHIS should consider industry practice in any further maintenance
surveillance effort. Animals unsuitable for slaughter exhibiting symptoms
not inconsistent with BSE should be sampled and their clinical signs
recorded. However, this cited industry practice results in rejected animals
not being made available to either APHIS or FSIS veterinarians for their
observation and identification of clinical signs exhibited ante mortem.
Although these animals may be sampled later at other collection sites, the
animals are provided post mortem without information as to relevant clinical
signs exhibited ante mortem. For these reasons, we believe APHIS needs to
USDA/OIG-A/50601-10-KC Page 27
observe these animals ante mortem when possible to assure the animals from
the target population are ultimately sampled and the clinical signs
evaluated.
snip…
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
APHIS-2006-0041-0006 TSE advisory committee for the meeting December 15,
2006
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8
Attachment to Singletary comment
January 28, 2007
Greetings APHIS,
I would kindly like to submit the following to ;
BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES
[Docket No. APHIS-2006-0041] RIN 0579-AC01
[Federal Register: January 9, 2007 (Volume 72, Number 5)]
[Proposed Rules]
[Page 1101-1129]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr09ja07-21]
http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8152
BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS
DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01
Date: January 9, 2007 at 9:08 am PST
http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f3412
Thursday, January 31, 2008
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform
Encephalopathy Prion Strain
J. Virol. doi:10.1128/JVI.02561-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed
Authors/Institutions. All Rights Reserved.
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform
Encephalopathy Prion Strain
Qingzhong Kong*, Mengjie Zheng, Cristina Casalone, Liuting Qing, Shenghai
Huang, Bikram Chakraborty, Ping Wang, Fusong Chen, Ignazio Cali, Cristiano
Corona, Francesca Martucci, Barbara Iulini, Pierluigi Acutis, Lan Wang,
Jingjing Liang, Meiling Wang, Xinyi Li, Salvatore Monaco, Gianluigi Zanusso,
Wen-Quan Zou, Maria Caramelli, and Pierluigi Gambetti*
Department of Pathology, Case Western Reserve University, Cleveland, OH
44106, USA; CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy;
Department of Neurological and Visual Sciences, University of Verona, 37134
Verona, Italy
* To whom correspondence should be addressed. Email: qxk2@case.edu.
pxg13@case.edu.
Abstract
snip…
These results suggest that, in humans, BASE is a more virulent BSE strain
and likely lymphotropic.
snip…
SEE FULL TEXT ;
http://jvi.asm.org/cgi/content/abstract/JVI.02561-07v1?papetoc
http://cjdmadcowbaseoct2007.blogspot.com/2008/01/evaluation-of-human-transmission-risk.html
http://cjdmadcowbaseoct2007.blogspot.com/
Thursday, January 31, 2008
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the 99th
meeting held on 14th December 2007
snip…
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION
40. The Chair explained that the purpose of the question and answer
session was to give members of the public an opportunity to ask
questions related to the work of SEAC. Mr Terry Singeltary
(Texas, USA) had submitted a question prior to the meeting,
asking: “With the Nor-98 now documented in five different states so
far in the USA in 2007, and with the two atypical BSE H-base
13
© SEAC 2007
cases in Texas and Alabama, with both scrapie and chronic
wasting disease (CWD) running rampant in the USA, is there any
concern from SEAC with the rise of sporadic CJD in the USA from
”unknown phenotype”, and what concerns if any, in relations to
blood donations, surgery, optical, and dental treatment, do you
have with these unknown atypical phenotypes in both humans and
animals in the USA? Does it concern SEAC, or is it of no concern
to SEAC? Should it concern USA animal and human health
officials?”
41. A member considered that this question …………
snip… please see full text, sources, and comments here ;
http://seac992007.blogspot.com/2008/01/spongiform-encephalopathy-advisory.html
CJD TEXAS
http://cjdtexas.blogspot.com/
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in
the United States
http://cjdusa.blogspot.com/
Creutzfeldt Jakob Disease
http://creutzfeldt-jakob-disease.blogspot.com/
Creutzfeldt-Jakob Disease, Prion Protein Gene Codon 129VV, and a Novel PrPSc
Type in a Young British Woman
http://creutzfeldt-jakob-disease.blogspot.com/2008/01/creutzfeldt-jakob-disease-prion-protein.html
CJD QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/
ANIMAL HEALTH REPORT 2006 (BSE h-BASE EVENT IN ALABAMA, Scrapie, and CWD)
http://animalhealthreport2006.blogspot.com/
CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA
http://cjdmadcowbaseoct2007.blogspot.com/
Friday, January 11, 2008
CJD HUMAN TSE REPORT UK, USA, CANADA, and Mexico JANUARY 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/01/cjd-human-tse-report-uk-usa-canada-and.html
Friday, January 25, 2008
January 2008 Update on Feed Enforcement Activities to Limit the Spread of
BSE
http://madcowspontaneousnot.blogspot.com/2008/01/january-2008-update-on-feed-enforcement.html
http://madcowspontaneousnot.blogspot.com/
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA
http://madcowtesting.blogspot.com/
NOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007
http://nor-98.blogspot.com/
http://scrapie-usa.blogspot.com/
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734.
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Since this article does not have an abstract, we have provided the first 150
words of the full text and any section headings.
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.
Terry S. Singeltary, Sr
Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL
TEXT
http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -Page 1. J Freas, William From: Sent:
To:
Subject:
Terry S. SingeltarySr. [flounder@wt.net]
Monday, January 08,200l 3:03 PM freas …
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
Asante/Collinge et al, that BSE transmission to the 129-methionine genotype
can lead to an alternate phenotype that is indistinguishable from type 2
PrPSc, the commonest _sporadic_ CJD;
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm
DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen)USA: Loch in der MauerDie
BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas
verbotenes Tiermehl ins Rinderfutter - die Kontrollen der
Aufsichtsbehördensind lax.Link auf diesen Artikel im
Archiv:http://service.spiegel.de/digas/find?DID=18578755
“Its as full of holes as Swiss Cheese” says Terry Singeltary of the FDA
regulations. …
http://service.spiegel.de/digas/servlet/find/DID=18578755
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
thank you,
kindest regards,
I am sincerely,
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
February 6th, 2008 at 4:07 am
Really long cut and pastes like that are kind of hard to follow.
Could you summarize in a reader’s digest version?
February 6th, 2008 at 11:13 am
it’s taken me over 10 years to uncover the cover-up. so it would take me a long time to explain here, that’s why i posted the links. in short, we have been lied to about mad cow disease in the USA. it’s been here. there is more than one strain in N. America, and the only reason Canada has found more cases, is the simple fact they are finding and _documenting_ cases. Canada’s feed ban is better. sporadic CJD (six documented phenotypes to date, with a recent _unknown_ phenotype documented in the USA). the h-BASE mad cow strain here in the USA is more virulent to humans than the UK BSE strain. the l-BASE mad cow strain has not been documented in the USA to date, but that does not say much. from the beginning of the enhanced BSE surveillance program, the testing was flawed, and the surveillance program itself was flawed (see links). the ruminant to rumiant feed ban i.e. mad cow feed, that was put into place August 4, 1997 would have helped. one problem, it nothing more than ink on paper, we are still feeding cows to cows and of that SRMs i.e. specified risk materials i.e. high risk organs, tissues etc.. the usda and fda have failed at every fire-wall. i said it in 2001 ;
DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen)
USA: Loch in der Mauer
Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas
verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehörden
sind lax.
Link auf diesen Artikel im Archiv:
http://service.spiegel.de/digas/find?DID=18578755
“Its as full of holes as Swiss Cheese” says Terry Singeltary of the FDA
regulations. …
http://service.spiegel.de/digas/servlet/find/DID=18578755
Thu Dec 6, 2007 11:38
FDA IN CRISIS MODE, AMERICAN LIVES AT RISK
http://www.cidrap.umn.edu/cidrap/content/fs/food-disease/news/dec0407fda.html
FDA SCIENCE AND MISSION AT RISK
http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4329b_02_01_FDA%20Report%20on%20Science%20and%20Technology.pdf
and the houston chronicle today stated that it would take the FDA, at present staffing level, 1,900 YEARS, to check every foreign food processor.
from the St. Louis Post-Dispatch
FALLOUT OF FDA NEGLECT
and then we wonder about the recent downer cattle that went to the school lunch programs and elderly, these are HIGH RISK MAD COWS. BUT, what are we feeding these cows still, one example;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES — CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
and 2006 was a banner year for mad cow protein animal feed in commerce. but there is not enough space here to list them all.
scrapie in sheep and goats is rampant in the USA, with the new atypical NOR-98 strain documented in 5 different states for the first time in 2007.
CWD in deer and elk is also rampant and spreading.
the significance of all this, human health risk, medical and surgical arena, second, third, fourth passage i.e. friendly fire exposure, only time will tell, but the transmission studies to date are very troublesome and disturbing. the incubation period of these different TSE, is what hinders research, and allows this agent to secretly spread for years. …
p.s. two old papers i always refer to;
Gerald Wells: Report of the Visit to USA, April-May 1989
snip…
The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised…
snip…
It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US…
snip…
3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ”Independent” with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_…
snip…
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988
Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle
R.F. Marsh* and G.R. Hartsough
•Department of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092
ABSTRACT
Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in
England.
INTRODUCTION
Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough
and Burger who demonstrated that the disease was transmissible with a long incubation
period, and that affected mink had a spongiform encephalopathy similar to that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965).
Because of the similarity between TME and scrapie, and the subsequent finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was
concluded that TME most likely resulted from feeding mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time provided
evidence that they may be different. Epidemiologic studies on previous incidences of
TME indicated that the incubation periods in field cases were between six months and
one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be
transmitted to mink in less than one year.
To investigate the possibility that TME may be caused by a (particular strain of
scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie
agent, including their sheep or goat sources, were inoculated into a total of 61 mink.
Only one mink developed a progressive neurologic disease after an incubation period of
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused
by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent
from an unidentified source.
OBSERVATIONS AND RESULTS
A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were “acting funny”, and some had died. At this time, we
visited the farm and found that approximately 10% of all adult mink were showing
typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over
their _backs like squirrels. These signs were followed by progressive deterioration of
neurologic function beginning with locomoior incoordination, long periods of somnolence
in which the affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over the past 12-18
months. The rancher was a “dead stock” feeder using mostly (>95%) downer or dead dairy
cattle and a few horses. Sheep had never been fed.
Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after incubation
periods of four months. To investigate the possible involvement of cattle in this disease
cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally
with a brain suspension from affected mink. Each developed a fatal spongiform
encephalopathy after incubation periods of 18 and 19 months.
DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle and
we have alerted bovine practitioners that there may exist an as yet unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new
bovine spongiform encephalopathy has recently been reported in England (Wells et al.,
1987), and investigators are presently studying its transmissibility and possible
relationship to scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be
confused with rabies in the United Stales and not be diagnosed. Presently, brains from
cattle in the United States which are suspected of rabies infection are only tested with
anti-rabies virus antibody and are not examined histopathologically for lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no agent-
specific proteins or nucleic acids identified for these transmissible neuropathogens, one
means of distinguishing them is by animal passage and selection of the biotype which
grows best in a particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral
backpassage of the experimental bovine agent resulted in incubations of only four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine passage.
Mink fed infected bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.
ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United
States Department of Agriculture. The authors also wish to acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.
REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.
MARSH
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
kindest regards,
terry
February 6th, 2008 at 12:28 pm
That looks like the same cut and paste. Now I’m beginning to think this is spam.