GAO
EMERGING ANIMAL DISEASES
Actions Needed to Better Position USDA to Address Future Risks
Report to the Chairman, Committee on Energy and Commerce, House of
Representatives December 2015 GAO-16-132
What GAO Found
The U.S. Department of Agriculture (USDA) did not take regulatory action during the initial response to the outbreaks of Swine Enteric Coronavirus Diseases (SECD) beginning in May 2013, when an outbreak was first detected, because the agency did not believe then that such action was necessary. Instead, USDA initially supported swine industry-led efforts. Without regulatory action, such as requiring reporting of infected herds, USDA had limited information about the location of the first infected herds. In addition, USDA officials acknowledged that USDA did not follow its guidance that calls for conducting epidemiological investigations at the onset of outbreaks. As a result, USDA did not conduct timely investigations of the premises with the first infected herds, and the source of disease will likely never be determined. Further, USDA does not have a process to help ensure the guidance is followed. Without such a process, USDA lacks reasonable assurance that the guidance will be followed in the future.
In June 2014, amid concerns about the spread of SECD, USDA issued a federal order requiring reporting of newly infected herds. As a result, USDA has more accurate information about the number and location of such herds, and SECD have been confirmed in 28 U.S. states, as shown below. USDA also provided funding to help manage the diseases.
Confirmed Swine Enteric
Coronavirus Diseases from June 5, 2014 to September 5, 2015
To help improve its future response to SECD and other emerging animal diseases—those not known to exist in the United States or which have changed to become a threat—USDA has drafted new guidance. However, it has not defined key aspects of its response such as roles and responsibilities, which according to its strategic plan, are key components of successful collaboration to protect animal health. Without a clearly defined response to such emerging animal diseases, response efforts could be slowed.
Why GAO Did This Study
Pork is consumed more than any other meat worldwide, and there are numerous other products made with ingredients from pigs, including medical products, such as insulin to treat diabetes. The United States is the world's third-largest producer of pork products. USDA estimated that U.S. pork exports in 2014 were valued at over $6 billion. Two lethal, highly contagious diseases in pigs emerged in the United States in 2013 and 2014, causing the deaths of millions of pigs. The two emerging diseases are collectively known as SECD.
GAO was asked to review federal actions to address SECD outbreaks. This report examines (1) the initial response to the SECD outbreaks, (2) USDA's subsequent actions to manage SECD, and (3) steps USDA has taken to improve its future response to emerging animal diseases. GAO analyzed USDA efforts to collect data about the number and location of infected herds; reviewed federal regulations and USDA animal disease response guidance; and interviewed USDA, state, and industry stakeholders involved in the response and control efforts.
What GAO Recommends
GAO recommends that USDA develop a process to help ensure its guidance for investigation of animal diseases is followed and clarify and document how it will respond to emerging diseases, including defining roles and responsibilities. USDA generally agreed with GAO's recommendations.
For more information, contact John Neumann at (202) 512-3841 or neumannj@gao.gov.
LOL!
time and time and time again, the USDA is a failed entity, just like the
OIE. God protect the industry at all cost, including human and animal health.
how many GAO reports, year after year after year, from the GAO, addressing
these same failures with TSE Prion disease, before something is done?
I was disgusted and very disturbed that in this report, Report to the
Chairman, Committee on Energy and Commerce, House of Representatives December
2015 GAO-16-132, Transmissible Spongiform Encephalopathy TSE Prion was not even
mentioned. very, very, disturbing. like it or not, the TSE prion, this dangerous
pathogen has not gone anywhere. ...TSS
Research article
Transmission of sheep-bovine spongiform encephalopathy to pigs
Carlos Hedman1, Rosa Bolea1*, Belén Marín1, Fabien Cobrière4, Hicham
Filali1, Francisco Vazquez2, José Luis Pitarch1, Antonia Vargas1, Cristina
Acín1, Bernardino Moreno1, Martí Pumarola3, Olivier Andreoletti4 and Juan José
Badiola1
* Corresponding author: Rosa Bolea rbolea@unizar.es
Author Affiliations
1 Veterinary Faculty, Centro de Investigación en Encefalopatías y
Enfermedades Transmisibles Emergentes (CIEETE), Universidad de Zaragoza,
Zaragoza, 50013, Spain
2 Veterinary Hospital, Universidad de Zaragoza, Zaragoza, 50013, Spain
3 Veterinary Faculty, Department of Animal Medicine and Surgery,
Universitat Autònoma de Barcelona, Barcelona, 08193, Spain
4 UMR INRA ENVT 1225, Interactions Hôtes Agents Pathogènes, Ecole Nationale
Vétérinaire de Toulouse, Toulouse, 31076, France
For all author emails, please log on.
Veterinary Research 2016, 47:14 doi:10.1186/s13567-015-0295-8
The electronic version of this article is the complete one and can be found
online at: http://www.veterinaryresearch.org/content/47/1/14
Received: 15 May 2015 Accepted: 21 September 2015 Published: 7 January 2016
© 2016 Hedman et al.
Open Access
This article is distributed under the terms of the Creative Commons
Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/),
which permits unrestricted use, distribution, and reproduction in any medium,
provided you give appropriate credit to the original author(s) and the source,
provide a link to the Creative Commons license, and indicate if changes were
made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/)
applies to the data made available in this article, unless otherwise stated.
Abstract
Experimental transmission of the bovine spongiform encephalopathy (BSE)
agent has been successfully reported in pigs inoculated via three simultaneous
distinct routes (intracerebral, intraperitoneal and intravenous). Sheep derived
BSE (Sh-BSE) is transmitted more efficiently than the original cattle-BSE
isolate in a transgenic mouse model expressing porcine prion protein. However,
the neuropathology and distribution of Sh-BSE in pigs as natural hosts, and
susceptibility to this agent, is unknown. In the present study, seven pigs were
intracerebrally inoculated with Sh-BSE prions. One pig was euthanized for
analysis in the preclinical disease stage. The remaining six pigs developed
neurological signs and histopathology revealed severe spongiform changes
accompanied by astrogliosis and microgliosis throughout the central nervous
system. Intracellular and neuropil-associated pathological prion protein (PrP Sc
) deposition was consistently observed in different brain sections and
corroborated by Western blot. PrP Sc was detected by immunohistochemistry and
enzyme immunoassay in the following tissues in at least one animal: lymphoid
tissues, peripheral nerves, gastrointestinal tract, skeletal muscle, adrenal
gland and pancreas. PrP Sc deposition was revealed by immunohistochemistry alone
in the retina, optic nerve and kidney. These results demonstrate the efficient
transmission of Sh-BSE in pigs and show for the first time that in this species
propagation of bovine PrP Sc in a wide range of peripheral tissues is possible.
These results provide important insight into the distribution and detection of
prions in non-ruminant animals.
Introduction Transmissible spongiform encephalopathies (TSE) are chronic
neurodegenerative disorders that affect humans and animals and are associated
with the accumulation of an abnormal isoform (PrP Sc ) of the cellular prion
protein (PrP C ) in the central nervous system (CNS) [1]. TSE are characterized
by spongiform changes in the grey matter accompanied by astrocytosis and
microgliosis [2]–[4]. The new variant of Creutzfeldt-Jakob disease (nvCJD) in
humans [5] has been linked with the consumption of bovine spongiform
encephalopathy (BSE) contaminated meat or meat products during the BSE epidemic
in the UK and elsewhere. Moreover, one BSE natural case in a goat in France [6]
and another one in the UK [7], [8] have been reported. Sheep and goats can also
be experimentally infected using homogenized brain from affected animals as
inocula [9]–[11]. While BSE infection is largely restricted to the nervous
system in cattle [12], [13], PrP Sc is widely distributed in the lymphoid
tissues of sheep experimentally infected with BSE [10], [14], suggesting that
infected sheep could constitute a secondary and more dangerous source of BSE
infection for other species, including humans [15]–[17].
TSE has not been reported in natural conditions in pigs [18], and there is
no evidence of BSE transmission between pigs fed with brain material from cattle
[19]. However, despite the existence of a strong transmission barrier, signs of
TSE have been reported in pigs challenged simultaneously with BSE-derived
material via intraperitoneal, intravenous and intracerebral administration
[20]–[22]. Those studies demonstrated pathological changes and PrP Sc deposition
in the CNS, but reported no evidence of PrP Sc distribution in other organs.
Given the possible lifting of the European Union’s ban on feeding pigs and
poultry with animal meal, it is vital that TSE transmission be studied in
supposedly resistant species, such as swine, that form part of the human food
chain. Pigs are the source of a wide range of food products, and pork is one of
the most widely eaten meats in the world. Blood is frequently collected during
slaughter for blood sausage production and natural sausage casings are almost
exclusively prepared from different parts of the alimentary tract of pigs. The
use of pigs as graft donors is also a cause for concern, given a reported case
of CJD type 1 in a recipient of a porcine dura-mater graft [23]. It has also
been demonstrated that BSE experimentally passaged in sheep (Sh-BSE) homozygous
for the A 136 R 154 Q 171 allele of ovine prion protein (PrP) exhibits altered
pathobiological properties due to a decreased polymorphism barrier [24]. The
virulence of Sh-BSE in transgenic mice expressing porcine [15] and human PrP
[16], [25] is enhanced with respect to the original cattle BSE prion isolate.
This study is the first to describe the tissue distribution of PrP Sc in
pigs experimentally infected with BSE previously passaged in sheep, as well as
the clinical and neuropathological consequences.
snip...
Discussion This study was aimed at investigating the susceptibility and
neuropathological features of pigs intracerebrally inoculated with the BSE agent
after passage in sheep, as well as describing the PrP Sc distribution in
peripheral tissues in this species.
In the present study, seven pigs were intracerebrally inoculated with 0.5
mL of 10% Sh-BSE homogenate. Except in one animal (P-7), which was euthanized
for preclinical analysis, the transmission rate was 100%, with an incubation
period range of 77–109 wpi. Two previous studies in which bovine BSE has been
transmitted to pigs, reported 87.5% and 20% of rate attacks, with incubation
period ranges of 74–163 and 148–175 wpi, respectively [19], [20]. Sh-BSE
infected pigs show slightly shorter incubation periods. However, it is not
possible to compare the incubation period of our inoculated pigs with respect to
the incubation period found in the studies mentioned above, due to the lack of
titration of the original inoculum. Moreover, the incubation period could also
be modified in TSE due to the species barrier, which is modulated by specific
polymorphisms of the PRNP gene and plays a key role in susceptibility to prion
disease in other species such as sheep [35], [36], and goats [37]. Although some
studies show that there are no differences in the sequence of the porcine PRNP
gene [38]–[40], the possibility of changes in other regions of the gene or the
involvement of other genes in the incubation periods of BSE in pigs should not
be excluded. In addition, the restricted number of animals used does not allow
comparing difference on rate attacks in previous studies with the present
report. However, transmissible studies in porcine PRNP transgenic mice (Tgpo)
has demonstrated that the Sh-BSE agent reached rate attack of 100% and lower
survival time when compared to the original bovine BSE (19%) and other BSE
isolates at first passage [15]. At two subsequent passages, the transmission
rate of both Sh-BSE and bovine BSE was reported to be similar (100%) but always
with a lower survival time of the Sh-BSE infected mice [15]. Recent studies have
demonstrated an increase in the PrP-converting potency of Sh-BSE caused by
decreases in polymorphism barriers [24] and other specific cellular factors
[25], allowing Sh-BSE to be transmitted more efficiently than cattle BSE to
other species [16], [17] including supposedly less susceptible hosts such as
pigs [15]. The current study was in agreement with previous reports [20]–[22]
involving intracerebral inoculation of BSE prions to pigs demonstrating that
this species is susceptible to BSE. However, it is still unknown if pigs can
succumb to BSE after oral exposure which is the most likely route of inoculation
under natural conditions.
The clinical signs observed in the present study were similar to those
described in BSE-infected pigs [20]. Animals initially showed progressive
confusion, followed by motor deficits [19]. The behavioral and sensory changes
were also consistent with those observed in cattle infected naturally [41] and
experimentally with BSE [12]. The minimal neuropil vacuoles found in the control
pig are in total agreement with previous studies [21] and apparently does not
represent a clinical significant change [20]. The main pathological changes
observed were neuropil spongiosis, intraneuronal vacuolation and PrP Sc
deposition, all of which are characteristic of TSE [41]. The lesion distribution
pattern resembled that described previously in experimentally BSE- infected pigs
[21] and cattle [12]; the thalamus was the most affected area, followed by the
cerebellar and cerebral cortices, with the mildest effect observed in the spinal
cord. PrP Sc deposits were identified in the CNS of all clinically affected
pigs. PrP Sc deposits were typically associated with lesions in the fourth and
fifth layers of the cerebral cortex. Intracellular (ITNR, ITAS and ITMG) and
particulate/coalescing type PrP Sc deposition were the most commonly observed
patterns in the different CNS samples, in line with previous findings in sheep
[29], [30] and pigs [21] experimentally infected with BSE. Similarities in the
PrP Sc deposition types and distribution pattern could be explained by the high
stability of the BSE agent reported for different breeds and different genotypes
of the prion protein gene (PRNP) in sheep [30]. In addition, the porcine PRNP
gene has been described to be very homogenous [38]–[40].
The glial reaction in all affected pigs was characterized by marked
astrocytosis and microgliosis. Astrocytosis was diffusely distributed throughout
the brain of affected pigs, perhaps caused by the accumulation of PrP Sc or by
cytokines secreted from astroglial or microglial cells [42]. Microgliosis was
present in the deeper layers of the gray matter in the cerebral cortex, which
also showed vacuolation and PrP Sc deposition, in accordance with previous
findings in mice [43]. The most extreme microglial activation was observed in
the hippocampus of all affected pigs, as previously described for CJD [44].
Numerous astrocytic processes and reactive microglia have been described in pigs
experimentally infected with BSE [45]. Our results suggest that astrogliosis and
microgliosis are common neuropathological features of Sh-BSE infection in pigs,
as described for TSE in other species [28], [43], [45]–[47].
Histopathological changes indicative of retinal degeneration were observed
in all clinically affected pigs. This has not been previously described in pigs
experimentally infected with BSE. Neuronal vacuolation in the GCL and
disorganization in the plexiform and nuclear layers have been reported in both
experimental [48] and natural scrapie infections in sheep [49] and goats [50],
chronic wasting disease (CWD) in mule deer [51] and in CJD-infected mice [52].
IHC revealed higher levels of PrP Sc in the retina than in the optic nerve,
where staining was less intense and more irregularly distributed, as described
in both sCJD and nvCJD [53]. The presence of PrP Sc in the optic nerve and
retina is consistent with the centrifugal spread of the agent from the brain,
presumably via the optic nerve [52]. This may indicate the existence of other
routes of PrP Sc migration to the retina (e.g., via the extracellular space
[54], the ad-axonal route along the optic nerve, or both [55]). Other authors
have suggested that the spread occurs from the subarachnoid space into the
perineural space of the optic nerve, and from there to the epichoroidal and
episcleral tissues of the eyeball [56]. Alternatively, the increased presence of
PrP Sc in the retina more than in the optic nerve could be attributed to the
higher presence of PrP c in the membranes of retinal neurons. Our detection of
PrP Sc in different retinal layers is in accordance with previous observations
in TSE in mice [52], feline spongiform encephalopathy (FSE) [57], scrapie [49],
CWD [51], BSE [56] and in patients with sporadic and nvCJD [53].
Western blot revealed a characteristic 3-band pattern that clearly differed
from the original inoculum, with a predominant monoclycosylated band. This
finding is consistent with previous Western blot findings in BSE-infected pigs
[58]. Our results reinforce the hypothesis that this particular signature is
associated with the porcine PrP c properties described in Tgpo mice [15].
The IDEXX enzyme immunoassay, which is not validated for PrP sc in pigs,
detected PrP Sc in samples that tested positive in other postmortem assays, but
detected no PrP sc in negative control tissues. Analysis of peripheral tissues
revealed widespread dissemination of PrP Sc in many organs other than the CNS.
This finding suggests that unlike in cattle where BSE is confined mainly in the
nervous system, in the pig, BSE prions can propagate in peripheral tissues as
reported in sheep [59]–[61]. However, it is not possible to ascertain that the
peripheral distribution of the agent is due to centrifugal dissemination from
the brain through the nerves as it is also probable that during an ic challenge
part of the inoculum enters into the blood circulation and can be disseminated
to the periphery where it can propagate in target tissues [62].
PrP Sc deposition in brachial and sciatic nerves has also been described in
cattle experimentally infected with L-type BSE [63] and in BSE-infected sheep
[64].
Immunohistochemistry demonstrated the presence of PrP Sc in the
lymphoreticular system of our Sh-BSE infected pigs. The assay revealed sporadic
intracytoplasmic accumulation within the tingible body macrophages in some lymph
nodes, findings that were subsequently corroborated by IDEXX, in good agreement
with previous findings in sheep experimentally infected with BSE [64]. In
contrast to our findings, previous studies reported no infectivity of lymphoid
tissues in BSE-infected pigs [19]. No PrP Sc was detected in the spleen or GALT
of our pigs, in line with previous studies of BSE-infected cattle [65] and FSE
[57].
PrP Sc accumulation in the gastrointestinal tract of Sh-BSE infected pigs
has not been described in similar experiments using this species. We observed
PrP Sc deposition in the myenteric plexi without apparent morphological
alterations of the enteric neurons, as seen in cattle experimentally infected
with BSE [65]. This finding is indicative of a potential centrifugal spread of
the Sh-BSE agent from the CNS via the vagus nerve to the peripheral nervous
system, and may account for the large deposits of PrP Sc observed in the dorsal
motor nucleus of the vagus nerve in the medulla oblongata.
We observed PrP Sc deposition in nerve fibers of the oculomotor muscle in
two pigs. In cattle naturally infected with BSE [66], PrP Sc has been detected
in intramuscular nerve fibers and muscle spindles. Although we found no PrP Sc
in the oculomotor muscle of any other clinically affected pigs, positive
labeling was observed in the oculomotor nuclei in the mesencephalon of all
clinically affected pigs.
Pancreatic PrP Sc staining was observed in 5 pigs. Analysis of pancreatic
nervous tissue has revealed PrP Sc deposition in the islets of Langerhans in
natural scrapie [34]. In natural BSE [56], PrP Sc deposition has been documented
in the nerve fibers of the adrenal gland. In agreement with previous findings in
natural scrapie [34], one pig showed PrP Sc immunolabeling in the medullary
region of the adrenal gland, associated with chromaffin cells, which are
considered modified sympathetic postganglionic neurons. Similarly, the presence
of PrP Sc within the epithelial tubular cells of the convoluted tubules and the
collecting ducts in the kidney in one pig has been described in FSE [67],
suggesting possible prionuria.
In addition to the large amount of PrP Sc observed in the CNS of
Sh-BSE-infected pigs, PrP Sc was widely distributed in the peripheral tissues,
although the extent of this distribution varied between animals. This variation
may be related to the distribution of PrP Sc within individual organs, the exact
anatomical location points at which samples were collected, and the detection
limits of the techniques used. More sensitive studies, such as in vitro protein
misfolding cyclic amplification (PMCA) and mouse bioassays will be needed to
clarify the distribution and infectivity of PrP Sc in peripheral tissues of
Sh-BSE infected pigs. These assays will most likely indicate a higher number of
PrP Sc -positive peripheral organs.
Comparison with previous studies of cattle-BSE in pigs revealed that the
incubation period of Sh-BSE in our pigs was generally shorter [20], [21] and
that PrP Sc was present in more peripheral tissue types [19]. We believe that
these differences may be due to a modification in the pathogenicity of the
cattle-BSE agent caused by its prior passage in sheep, as previously described
in TgPo mice [15]. However, studies of natural routes of transmission (e.g.,
oral) will be required to determine the real susceptibility of pigs to the
Sh-BSE agent.
Saturday, January 9, 2016
Transmission of sheep-bovine spongiform encephalopathy to pigs
Research article
Thursday, February 19, 2015
Inspections Circumvented for Condemned Cows STATEMENT OF THE HONORABLE
PHYLLIS K. FONG INSPECTOR GENERAL
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
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...see full text ;
Thursday, October 22, 2015
Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad
cow disease USDA and what really happened
Comments on technical aspects of the risk assessment were then submitted to
FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary.
This document provides itemized replies to the public comments received on
the 2005 updated Harvard BSE risk assessment. Please bear the following points
in mind:
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 to APHIS FDA USDA et al ;
To: agsec@usda.gov
Cc: john.clifford@aphis.usda.gov; usaha@usaha.org; jmeng@cpfbeef.com;LAVET22@aol.com Phyllis.Fong@usda.gov
Sent: Tuesday, May 29, 2007 2:07 PM
Subject: USDA VS CREEKSTONE BSE/BASE/TSE TESTING Civil Action No. 06-0544 (JR) May 27, 2007
Honorable Michael Johanns Secretary of Agriculture U.S. Department of Agriculture Room 200 Jamie Whitten Federal Building Washington, D.C. 20250 CC Honorable Judge James Robertson U.S. District Court 333 Constitution Ave. North West Washington, D. C. 20001 Subject: Request to let the Creekstone vs. USDA court decision stand.
Ref: Letter from United States Animal Health Association, dated May 22, 2007
Dear Mr. Secretary et al : I am requesting that you allow the court decision in the Creekstone vs. USDA to stand so that Creekstone may begin testing the beef they process for BSE and or BASE and or any other TSE phenotype there of. WE must let them test since the USDA et al refuse to do so properly. This is not to say that there should be no strict TSE testing protocols. IF testing is to take place privately, there must be strict TSE testing protocol to assure the most up to date, sensitive, and validated tests are used, and used properly. These tests must be announced to the public in a timely manner at every step of the way, validated and confirmed by the federal government, Weybridge, and an independent third party consumer organization and there TSE expert of choice, in my opinion. My mother died from a exceedingly rare strain of sporadic CJD i.e. the Heidenhain Variant of CJD. My neighbors mother also lost his mother to a form of sporadic CJD exactly one year previously from the day my mother died. BOTH cases were confirmed by autopsy. There is new data out about the BASE atypical BSE, which pathologically is more related to a phenotype of sporadic CJD, than the nvCJD in humans from the UK. To continue to ignore these scientific findings with the old UKBSEnvCJD only theory is not justified by science anymore. It is not logical. The logic behind the reasons not to let test for TSE in the USA because of The Virus Serum Toxin Act of 1913 and or because of the recent letter from the USAHA (see letter below) bring forth, are totally bogus. NO one could screw the testing up any worse than the USDA has done in the past. The OIG and the GAO has shown this time and time again. The 2004 Enhanced BSE surveillance program where some 275,000+ cattle were tested for BSE was proven to be terribly flawed from the beginning. This documented time and time again. Even Paul Brown, known and respected TSE scientist, former TSE expert for the CDC said he had ''absolutely no confidence in USDA tests before one year ago'', and this was on March 15, 2006 ; "The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that." Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive. USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general. "Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...
snip...end
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM "
Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."
OR, what the Honorable Phyllis Fong of the OIG found ;
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 http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
Mr. Johanns, The August 4, 1997
FDA BSE ruminant to ruminant feed ban was nothing more than ink on paper.
In 2007 alone, 10 MILLION plus pounds of banned blood laced MBM has already gone out into commerce for the feeding of banned product to cattle. yes, were still feeding cows banned BSE/BASE product in 2007, almost 10 years after the voluntary ban was put in place.
guess what, it aint working.
YOU and this Administration have failed terribly in protecting not only the consumer, but your precious commodity that you speak so highly of i.e. the beef industry. In your continued efforts to cover up the real mad cow problem in the USA, you have in fact only amplified it and continued it's spread, and in doing so, you have needlessly exposed millions to the TSE agent, from many different proven routes and sources. The only saving grace you have is the incubation period has been on your side. It will catch up. When it does, when the people finally figure all this out, when some of the millions you have needlessly exposed to this agent become clinical in the future, rest assured I will stand in line to see that you and your administration are convicted for murder. What you and this administration have done over the past 8 years is criminal, in my opinion. I have watched not only you, but the Bush administration thumb there nose to science for almost 8 years, all to protect the beef industry. The science was there, but you chose to ignore it, and even manipulated science with the bogus BSE MRR policy, all the while your were implementing that, you were covering up another mad cow in Texas.
But thanks to the Honorable Phyllis Fong of the OIG, and an act of Congress, that mad cow was finally proven positive, unlike the other stumbling and staggering mad cow that was rendered without any test at all in Texas, but by then you had succeeded in the BSE MRR policy, the legal trading of all strains of TSE globally. You and this administration have done the same thing the UK did when they poisoned the globe with there exporting of BSE, except you made it legal now with the BSE MRR policy, and now we are dealing with BASE, a strain that is more virulent to humans. what happens when it mutates again?
When cwd deer and elk and there different phenotypes have all been rendered into feed, along with scrapie infected sheep in the USA, and a few TME to top that off, it will be a most interesting recipe will it not, and an interesting case study for humans for decades to come. sadly though, with the recent pet food scandal, and the deaths there of, we have learned a few things. one, that the elderly are expendable, but cats, dogs, and adolescents are not. and that the problem of our feeding of food producing animals has been tainted for decades. and with the melamine scandal, as with the mad cow feed scandal, it's the same old song and dance by you and the Bush administration, everything is o.k., will not hurt you, cover-up and protect the industry at all cost, and this will be another part of your sad legacy in History Sir.
To not allow BSE/TSE testing in the USA, testing that will find, only proves our point, you have and will continue to cover up the real mad cow problem in the USA. and the world knows this. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
UNITED STATES ANIMAL HEALTH ASSOCIATION 8100 Three Chopt Road, Suite 203 P. O. BOX K227 RICHMOND, VIRGINIA 23288 804- 285-3210 FAX 804-285-3367 E-Mail: usaha@usaha.org Web Site: www.usaha.org May 22, 2007 Honorable Michael Johanns Secretary of Agriculture U.S. Department of Agriculture Room 200 Jamie Whitten Federal Building Washington, D.C. 20250
Dear Mr. Secretary: The United States Animal Health Association (USAHA), wishes to express its encouragement to you and the Department of Agriculture to appeal the litigation surrounding private testing for Bovine Spongiform Encephalopathy. We hope you will strongly consider this as you work with the Office of General Counsel on this suit. To support this appeal, we offer that this sets a detrimental precedence on USDA's ability to regulate disease and testing processes in animal agriculture. As we appreciate the entrepreneurial spirit of Creekstone, the larger scale implications could lead to devastating impacts for food animal production in this country as itrelates to animal health. We do feel that private testing could hamper animal health officials' ability to locate disease occurrences, and exercise proper practices to trace, control and eliminate them. As you are aware, there are a number of factors that raise concern among animal health leaders and diagnosticians. We encourage you to thoroughly consider those upon your decision to appeal. We do recognize this is now a matter of the courts, and trust that our ability to safeguard animal health is not compromised as a result of this litigation. Please let us know if there is any further support we can provide.
Sincerely, Lee M. Myers President, U.S. Animal Health Association Cc: Dr. John Clifford
===============================
USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN 18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.
snip...
64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.
snip...
http://www.seac.gov.uk/minutes/95.pdf
3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years. ***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.***
6:30 Close of Day One
http://www.healthtech.com/2007/tse/day1.asp
Cc: john.clifford@aphis.usda.gov; usaha@usaha.org; jmeng@cpfbeef.com;LAVET22@aol.com Phyllis.Fong@usda.gov
Sent: Tuesday, May 29, 2007 2:07 PM
Subject: USDA VS CREEKSTONE BSE/BASE/TSE TESTING Civil Action No. 06-0544 (JR) May 27, 2007
Honorable Michael Johanns Secretary of Agriculture U.S. Department of Agriculture Room 200 Jamie Whitten Federal Building Washington, D.C. 20250 CC Honorable Judge James Robertson U.S. District Court 333 Constitution Ave. North West Washington, D. C. 20001 Subject: Request to let the Creekstone vs. USDA court decision stand.
Ref: Letter from United States Animal Health Association, dated May 22, 2007
Dear Mr. Secretary et al : I am requesting that you allow the court decision in the Creekstone vs. USDA to stand so that Creekstone may begin testing the beef they process for BSE and or BASE and or any other TSE phenotype there of. WE must let them test since the USDA et al refuse to do so properly. This is not to say that there should be no strict TSE testing protocols. IF testing is to take place privately, there must be strict TSE testing protocol to assure the most up to date, sensitive, and validated tests are used, and used properly. These tests must be announced to the public in a timely manner at every step of the way, validated and confirmed by the federal government, Weybridge, and an independent third party consumer organization and there TSE expert of choice, in my opinion. My mother died from a exceedingly rare strain of sporadic CJD i.e. the Heidenhain Variant of CJD. My neighbors mother also lost his mother to a form of sporadic CJD exactly one year previously from the day my mother died. BOTH cases were confirmed by autopsy. There is new data out about the BASE atypical BSE, which pathologically is more related to a phenotype of sporadic CJD, than the nvCJD in humans from the UK. To continue to ignore these scientific findings with the old UKBSEnvCJD only theory is not justified by science anymore. It is not logical. The logic behind the reasons not to let test for TSE in the USA because of The Virus Serum Toxin Act of 1913 and or because of the recent letter from the USAHA (see letter below) bring forth, are totally bogus. NO one could screw the testing up any worse than the USDA has done in the past. The OIG and the GAO has shown this time and time again. The 2004 Enhanced BSE surveillance program where some 275,000+ cattle were tested for BSE was proven to be terribly flawed from the beginning. This documented time and time again. Even Paul Brown, known and respected TSE scientist, former TSE expert for the CDC said he had ''absolutely no confidence in USDA tests before one year ago'', and this was on March 15, 2006 ; "The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that." Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive. USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general. "Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...
snip...end
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM "
Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."
OR, what the Honorable Phyllis Fong of the OIG found ;
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 http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
Mr. Johanns, The August 4, 1997
FDA BSE ruminant to ruminant feed ban was nothing more than ink on paper.
In 2007 alone, 10 MILLION plus pounds of banned blood laced MBM has already gone out into commerce for the feeding of banned product to cattle. yes, were still feeding cows banned BSE/BASE product in 2007, almost 10 years after the voluntary ban was put in place.
guess what, it aint working.
YOU and this Administration have failed terribly in protecting not only the consumer, but your precious commodity that you speak so highly of i.e. the beef industry. In your continued efforts to cover up the real mad cow problem in the USA, you have in fact only amplified it and continued it's spread, and in doing so, you have needlessly exposed millions to the TSE agent, from many different proven routes and sources. The only saving grace you have is the incubation period has been on your side. It will catch up. When it does, when the people finally figure all this out, when some of the millions you have needlessly exposed to this agent become clinical in the future, rest assured I will stand in line to see that you and your administration are convicted for murder. What you and this administration have done over the past 8 years is criminal, in my opinion. I have watched not only you, but the Bush administration thumb there nose to science for almost 8 years, all to protect the beef industry. The science was there, but you chose to ignore it, and even manipulated science with the bogus BSE MRR policy, all the while your were implementing that, you were covering up another mad cow in Texas.
But thanks to the Honorable Phyllis Fong of the OIG, and an act of Congress, that mad cow was finally proven positive, unlike the other stumbling and staggering mad cow that was rendered without any test at all in Texas, but by then you had succeeded in the BSE MRR policy, the legal trading of all strains of TSE globally. You and this administration have done the same thing the UK did when they poisoned the globe with there exporting of BSE, except you made it legal now with the BSE MRR policy, and now we are dealing with BASE, a strain that is more virulent to humans. what happens when it mutates again?
When cwd deer and elk and there different phenotypes have all been rendered into feed, along with scrapie infected sheep in the USA, and a few TME to top that off, it will be a most interesting recipe will it not, and an interesting case study for humans for decades to come. sadly though, with the recent pet food scandal, and the deaths there of, we have learned a few things. one, that the elderly are expendable, but cats, dogs, and adolescents are not. and that the problem of our feeding of food producing animals has been tainted for decades. and with the melamine scandal, as with the mad cow feed scandal, it's the same old song and dance by you and the Bush administration, everything is o.k., will not hurt you, cover-up and protect the industry at all cost, and this will be another part of your sad legacy in History Sir.
To not allow BSE/TSE testing in the USA, testing that will find, only proves our point, you have and will continue to cover up the real mad cow problem in the USA. and the world knows this. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
UNITED STATES ANIMAL HEALTH ASSOCIATION 8100 Three Chopt Road, Suite 203 P. O. BOX K227 RICHMOND, VIRGINIA 23288 804- 285-3210 FAX 804-285-3367 E-Mail: usaha@usaha.org Web Site: www.usaha.org May 22, 2007 Honorable Michael Johanns Secretary of Agriculture U.S. Department of Agriculture Room 200 Jamie Whitten Federal Building Washington, D.C. 20250
Dear Mr. Secretary: The United States Animal Health Association (USAHA), wishes to express its encouragement to you and the Department of Agriculture to appeal the litigation surrounding private testing for Bovine Spongiform Encephalopathy. We hope you will strongly consider this as you work with the Office of General Counsel on this suit. To support this appeal, we offer that this sets a detrimental precedence on USDA's ability to regulate disease and testing processes in animal agriculture. As we appreciate the entrepreneurial spirit of Creekstone, the larger scale implications could lead to devastating impacts for food animal production in this country as itrelates to animal health. We do feel that private testing could hamper animal health officials' ability to locate disease occurrences, and exercise proper practices to trace, control and eliminate them. As you are aware, there are a number of factors that raise concern among animal health leaders and diagnosticians. We encourage you to thoroughly consider those upon your decision to appeal. We do recognize this is now a matter of the courts, and trust that our ability to safeguard animal health is not compromised as a result of this litigation. Please let us know if there is any further support we can provide.
Sincerely, Lee M. Myers President, U.S. Animal Health Association Cc: Dr. John Clifford
===============================
USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN 18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.
snip...
64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.
snip...
http://www.seac.gov.uk/minutes/95.pdf
3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years. ***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.***
6:30 Close of Day One
http://www.healthtech.com/2007/tse/day1.asp
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to then Central
Bureau............
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
Report to Congressional Requesters: February 2005: Mad Cow Disease:
FDA's Management of the Feed Ban Has Improved, but Oversight Weaknesses
Continue to Limit Program Effectiveness:
[Hyperlink, http://www.gao.gov/cgi-bin/getrpt?GAO-05-101]:
January 2002 MAD COW DISEASE Improvements in the Animal Feed Ban and Other
Regulatory Areas Would Strengthen U.S. Prevention Efforts GAO-02-183
February 2005 MAD COW DISEASE
FDA’s Management of
the Feed Ban Has
Improved, but
Oversight Weaknesses
Continue to Limit
Program Effectiveness
GAO-05-101
What GAO Found
United States Government Accountability Office
Why GAO Did This Study
Highlights
Accountability Integrity Reliability
www.gao.gov/cgi-bin/getrpt?GAO-05-101.
To view the full product, including the scope
and methodology, click on the link above.
For more information, contact Robert A.
Robinson at (202) 512-3841 or
robinsonr@gao.gov.
Highlights of GAO-05-101, a report to
congressional requesters
February 2005
MAD COW DISEASE
FDA’s Management of the Feed Ban Has
Improved, but Oversight Weaknesses
Continue to Limit Program Effectiveness
FDA has made needed improvements to its management and oversight of
the
feed-ban rule in response to GAO’s 2002 report, but program
weaknesses
continue to limit the effectiveness of the ban and place U.S. cattle at
risk of
spreading BSE. Improvements made include FDA establishing a uniform
method of conducting compliance inspections and training FDA
inspectors,
as well as state inspectors who carry out inspections under agreements
with
FDA, on the new method. FDA also implemented new data-entry
procedures
that are designed to more reliably track feed-ban inspection results.
Consequently, FDA has a better management tool for overseeing
compliance
with the feed-ban rule and a data system that better conforms to
standard
database management practices. However, various program weaknesses
continue to undermine the nation’s firewall against BSE. For example:
• FDA acknowledges that there are more feed manufacturers and
transporters, on-farm mixers, and other feed industry businesses that
are
subject to the feed ban than the approximately 14,800 firms inspected
to
date; however, it has no uniform approach for identifying additional
firms.
• FDA has not reinspected approximately 2,800, or about 19 percent,
of
those businesses, in 5 or more years; several hundred are potentially
high risk. FDA does not know whether those businesses now use
prohibited material in their feed.
• FDA’s feed-ban inspection guidance does not include instructions to
routinely sample cattle feed to test for potentially prohibited material
as
part of the compliance inspection. Instead, it includes guidance for
inspectors to visually examine facilities and equipment and review
invoices and other documents.
• Feed intended for export is not required to carry a caution label "Do
not
feed to cattle or other ruminants," when the label would be required
if
the feed were sold domestically. Without that statement, feed
containing
prohibited material could be inadvertently or intentionally diverted
back
to U.S. cattle or given to foreign cattle.
• FDA has not always alerted USDA and states when it learned that
cattle
may have been given feed that contained prohibited material. This
lapse
has been occurring even though FDA’s guidance calls for such
communication.
• Although research suggests that cattle can get BSE from ingesting even
a
small amount of infected material, inspectors do not routinely inspect
or
review cleanout procedures for vehicles used to haul cattle feed.
More than 5 million cattle across
Europe have been killed to stop the
spread of bovine spongiform
encephalopathy (BSE), commonly
called mad cow disease. Found in
26 countries, including Canada and
the United States, BSE is believed
to spread through animal feed that
contains protein from BSE-infected
animals. Consuming meat from
infected cattle has also been linked
to the deaths of about 150 people
worldwide. In 1997, the Food and
Drug Administration (FDA) issued
a feed-ban rule prohibiting certain
animal protein (prohibited
material) in feed for cattle and
other ruminant animals. FDA and
38 states inspect firms in the feed
industry to enforce this critical
firewall against BSE. In 2002, GAO
reported a number of weaknesses
in FDA’s enforcement of the feed
ban and recommended corrective
actions. This report looks at FDA’s
efforts since 2002 to ensure
industry compliance with the feed
ban and protect U.S. cattle.
What GAO Recommends
GAO recommends FDA, among
other things, develop procedures
for finding additional firms subject
to the feed-ban and using tests to
augment inspections. FDA said the
study was thorough but disagreed
on four of nine recommendations.
GAO continues to believe that,
given the discovery of BSE in North
America and the oversight gaps
described in the report, the
recommended actions are needed
to protect U.S. cattle from BSE.
snip...full text ;
What GAO Found United States Government Accountability Office Why GAO Did
This Study Highlights Accountability Integrity Reliability
www.gao.gov/cgi-bin/getrpt?GAO-05-549T. To view the full product, including the
scope and methodology, click on the link above. For more information, contact
Robert A. Robinson at (202) 512-3841 or robinsonr@gao.gov. Highlights of
GAO-05-549T, a testimony to the Subcommittee on the Federal Workforce and Agency
Organization, Committee on Government Reform, House of Representatives
May 17, 2005 OVERSEEING THE U.S. FOOD SUPPLY
Steps Should Be Taken to Reduce Overlapping Federal Inspections and Related
Activities
USDA and FDA have primary responsibility for overseeing the safety of the
U.S. food supply; the Environmental Protection Agency (EPA) and the National
Marine Fisheries Service also play key roles. In carrying out their
responsibilities, these agencies spend resources on a number of overlapping
activities, particularly inspection/enforcement, training, research, and
rulemaking, for both domestic and imported food. For example, both USDA and FDA
conduct similar inspections at 1,451 dual jurisdiction establishments—facilities
that produce foods regulated by both agencies, as shown below. To better manage
the fragmented federal system, these agencies have entered into at least 71
interagency agreements—about a third of them highlight the need to reduce
duplication and overlap or make efficient and effective use of resources. The
agencies do not take full advantage of these agreements because they do not have
adequate mechanisms for tracking them and, in some cases, do not fully implement
them. Selected industry associations, food companies, consumer groups, and
academic experts disagree on the extent of overlap, on how best to improve the
federal system, and on whether to consolidate food safety-related functions into
a single agency. However, they agreed that laws and regulations should be
modernized to more effectively and efficiently control food safety hazards. As
GAO recently reported, Canada, Denmark, Ireland, Germany, the Netherlands, New
Zealand, and the United Kingdom also had fragmented systems. These countries
took steps to consolidate food safety functions— each country modified its food
safety laws and established a single agency to lead food safety management or
enforcement of food safety legislation.
GAO has issued many reports documenting problems resulting from the
fragmented nature of the federal food safety system—a system based on 30 primary
laws. This testimony summarizes GAO’s most recent work on the federal system for
ensuring the safety of the U.S. food supply. It provides (1) an overview of food
safety functions, (2) examples of overlapping and duplicative inspection and
training activities, and (3) observations on efforts to better manage the system
through interagency agreements. It also provides information on other countries’
experiences with consolidation and the views of key stakeholders on possible
consolidation in the United States. What GAO Recommends In the past, GAO has
recommended that the Congress consider fundamental restructuring to ensure the
effective use of scarce government resources. In the report that the
Subcommittee is releasing today, GAO recognizes that, short of reorganization,
other improvements can be made to help reduce overlap and duplication and to
leverage existing resources. For example, the Food and Drug Administration (FDA)
could use existing authority to commission U.S. Department of Agriculture (USDA)
inspections of dual jurisdiction establishments.
snip...full text below
-------- Original Message --------
Subject: GAO September 2004 EMERGING INFECTIOUS DISEASE Review of State and
Federal Disease Surveillance Efforts GAO-04-877
Date: Mon, 01 Nov 2004 14:24:33 –0600
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy , NelliganJ@gao.gov, JarmonG@gao.gov
CC: cjdvoice@yahoogroups.com
Report to the Chairman, Permanent Subcommittee on Investigations, Committee
on Governmental Affairs, U.S. Senate United States Government Accountability
Office GAO September 2004 EMERGING INFECTIOUS DISEASES Review of State and
Federal Disease Surveillance Efforts GAO-04-877
snip...
Description of U.S. List of Nationally Notifiable Infectious Diseases, 2004
(no human TSE was listed...TSS)
snip...
Selected Worldwide Emerging Infectious Diseases
Variant Creutzfeldt-Jakob disease (vCJD) is a rare, degenerative, fatal
brain disorder in humans. It is believed that vCJD is contracted through the
consumption of cattle products contaminated with the agent of bovine spongiform
encephalopathy (BSE) or mad cow disease a slowly progressive, degenerative,
fatal disease affecting the central nervous system of adult cattle. There is no
known treatment of vCJD.
snip...end
1. Emerging Infectious Diseases: Review of State and Federal Disease
Surveillance Efforts. GAO-04-877, September 30. http://www.gao.gov/cgi-bin/getrpt?GAO-04-877
www.gao.gov/cgi-bin/getrpt?GAO-04-877.
To view the full product, including the scope and methodology, click on the
link above. For more information, contact Majorie Kanof at (202) 512-7119.
Highlights of GAO-04-877, a report to the Chairman, Permanent Subcommittee on
Investigations, Committee on Governmental Affairs, U.S. Senate September 2004
EMERGING INFECTIOUS DISEASES Review of State and Federal Disease Surveillance
Efforts The threat posed by infectious diseases has grown. New diseases, unknown
in the United States just a decade ago, such as West Nile virus and severe acute
respiratory syndrome (SARS), have emerged. To detect cases of infectious
diseases, especially before they develop into widespread outbreaks, local,
state, and federal public health officials as well as international
organizations conduct disease surveillance. Disease surveillance is the process
of reporting, collecting, analyzing, and exchanging information related to cases
of infectious diseases. In this report GAO was asked to examine disease
surveillance efforts in the United States. Specifically, GAO described (1) how
state and federal public health officials conduct surveillance for infectious
diseases and (2) initiatives intended to enhance disease surveillance. GAO
reviewed documents, such as policy manuals and reports related to disease
surveillance, and interviewed officials from selected federal departments and
agencies, including the Departments of Defense (DOD), Agriculture (USDA), and
Homeland Security (DHS) as well as the Food and Drug Administration (FDA), and
the Centers for Disease Control and Prevention (CDC). GAO conducted structured
interviews of state public health officials from 11 states. Surveillance for
infectious diseases in the United States comprises a variety of efforts at the
state and federal levels. At the state level, state health departments collect
and analyze data on cases of infectious diseases. These data are required to be
reported by health care providers and others to the state. State public health
departments verify reported cases of diseases, monitor disease incidence,
identify possible outbreaks within their state, and report this information to
CDC. At the federal level, agencies and departments collect and analyze disease
surveillance data and maintain disease surveillance systems. For example, CDC
uses the reports of diseases from the states to monitor national health trends,
formulate and implement prevention strategies, and evaluate state and federal
disease prevention efforts. FDA analyzes information on outbreaks of infectious
diseases that originate from foods that the agency regulates. Some federal
agencies and departments also fund and operate their own disease surveillance
systems and laboratory networks and have several means of sharing surveillance
information with local, state, and international public health partners. State
and federal public health officials have implemented a number of initiatives
intended to enhance disease surveillance, but challenges remain. For example,
officials have implemented and expanded syndromic surveillance systems, which
monitor the frequency and distribution of health-related symptoms among people
within a specific geographic area. Although syndromic surveillance systems are
used by federal agencies and departments and in all of the states whose
officials GAO interviewed, concerns have been raised about this approach to
surveillance. Specifically, syndromic surveillance systems are relatively costly
to maintain compared to other types of surveillance and are still largely
untested. Public health officials are also implementing initiatives designed to
enhance public health communications and disease reporting. For example, CDC is
working to increase the number of participants using its public health
communication systems. In addition, state public health departments and CDC are
implementing an initiative designed to make electronic disease reporting more
timely, accurate, and complete. However, the implementation of this initiative
is incomplete. Finally, federal public health officials have enhanced federal
coordination on disease surveillance and expanded training programs for
epidemiologists and other public health experts. In commenting on a draft of
this report, the Department of Health and Human Services (HHS) said the report
captures many important issues in surveillance. HHS also provided suggestions to
clarify the discussion.
Highlights - http://www.gao.gov/highlights/d04877high.pdf
Greetings GAO,
I am deeply disturbed by the fact that not only the USDA/FDA/CDC/APHIS, BUT
most dirturbing the GAO refuse to acknowledge ALL Human/Animal TSEs. With not
only BSE in cattle, you now have BASE in cattle, showing up in more and more
countries and we now have another atypical TSE, not sheep now, but a GOAT, that
is indistinguishable from BSE. THERE are atypical TSEs showing up in humans,
being documented as sporadic CJD, while we have a new TSE in CATTLE 'BASE' and
the title of the study speaks for itself;
Medical Sciences
Identification of a second bovine amyloidotic spongiform encephalopathy:
Molecular similarities with sporadic Creutzfeldt-Jakob disease
TO pour more gas on the fire we have other atyical TSEs that are going
ignored, and this is what got us in this mess. Please do not continue to make
the same mistakes. sporadic CJD does have routes and sources. THIS is why all
Human/Animal TSEs must be made reportable across the board. THERE is no other
answer...
How can you have this ;
> A notifiable disease is an infectious disease for which regular, >
frequent, and timely information on individual cases is considered >
necessary for the prevention and control of the disease...
THEN have this;
> The diseases that must be reported vary by state...
AND at the same time stop the spread of human/animal TSEs across the
board?
answer: you can't, and the agent continues to spread.
you must not continue to ignore the obvious; ...snip...end
OIG same old song and dance until 2008 ;
Safety and Security: Increasingly we have all come to realize that the
world
presents greater threats to our well being as individuals and a citizenry
in terms
of health and resources. Challenges such as those related to maintaining a
safe
food supply and protecting America’s plants and animals from invasive pests
are
critical. Thus, we have established as a strategic goal
"Support USDA in the
enhancement of safety and security measures to protect USDA and
agricultural resources and in related public health concerns." ...
•GAO-05-51 October 2004 FOOD SAFETY (over 500 customers receiving
potentially BSE contaminated beef)
-------- Original Message --------
Subject: USDA and FDA Need to Better Ensure Prompt and Complete Recalls of
Potentially Unsafe Food GAO-05-51
Date: Wed, 20 Oct 2004 13:40:01 -0500 From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy CC: cjdvoice@yahoogroups.com
October 2004 FOOD SAFETY USDA and FDA Need to Better Ensure Prompt and
Complete Recalls of Potentially Unsafe Food
snip...
Page 38 GAO-05-51 Food Recall Programs
To examine the voluntary recall of beef products associated with the
December 2003 discovery of an animal infected with BSE, we analyzed the
distribution lists USDA collected from companies and the verification checks it
conducted to develop a diagram illustrating the location and volume of recalled
beef that reached different levels of the distribution chain. We compared the
distribution lists and verification checks to identify how many customers listed
on the distribution lists did not receive the recalled beef and the number of
customers not listed on distribution lists that received the recalled beef. We
interviewed USDA and FDA staff involved with the recall to understand the timing
of recall actions and the challenges encountered during the recall.
To develop information on the 2002 recall of ground beef by a ConAgra plant
in Greeley, Colorado, we reviewed USDA’s recall file and other documents on the
recall. We also met with the department’s Office of Inspector General and
reviewed the Inspector General’s September 2003 report.1
We conducted our review from May 2003 through August 2004 in accordance
with generally accepted government auditing standards. 1U.S. Department of
Agriculture, Office of Inspector General, Great Plains Region Audit Report: Food
Safety and Inspection Service: Oversight of Production Process and Recall at
ConAgra Plant (Establishment 969), Report No. 24601-2-KC (September 2003).
Page 39 GAO-05-51 Food Recall Programs
Appendix II
Federal Actions Associated with the Discovery of an Animal in the United
States Infected with BSE Appendix II
On December 23, 2003, USDA announced that a cow in the state of Washington
had tested positive for BSE—commonly referred to as mad cow disease. This
appendix describes the actions USDA took to recall the meat and the actions FDA
took with respect to FDA-regulated products, such as animal feed and cosmetics,
made from rendered parts of the animal.
Beef Recall Was Triggered by a BSE Positive Sample from One Cow On December
9, 2003, the recalling company slaughtered 23 cows. USDA, in accordance with its
BSE surveillance policy at the time, took a sample of 1 cow that was unable to
walk, although the condition of the tested cow is now disputed. USDA did not
process the sample in its Ames, Iowa National Veterinary Services Laboratory in
an expedited manner because the cow did not show symptoms of neurological
disorder. USDA test results indicated a presumptive positive for BSE on December
23, 2003. Recall Begun in December 2003 Was Completed in March 2004
On December 23, 2003, after learning about the positive BSE test, USDA
headquarters notified the Boulder District Office, which is the field office
with jurisdiction over the recalling firm. The Boulder District began gathering
information about the recalling company’s product distribution. Field staff
telephoned the recalling company and were on-site at 7:00 p.m. The Boulder
District initially thought 3 days of the recalling company’s production would
have to be recalled, but further examination of facility cleanup and shipping
records revealed that it was only necessary to recall 1 day of production. USDA
recall staff convened at 9:15 p.m. and discussed the science related to BSE and
whether the recalling company’s cleanup practices were sufficient to limit the
recall to 1 day of production. Following USDA’s determination to conduct a Class
II recall—that is, the beef posed a remote possibility of adverse health
consequences—USDA contacted the recalling company to discuss recall details and
the press release. The press release and Recall Notification Report were
released that evening.
On December 24, 2003, USDA’s Food Safety and Inspection Service (FSIS) sent
inspectors to the recalling company’s primary customers to obtain secondary
customer distribution lists and product shipping records. USDA conducted 100
percent verification checks for this recall—it contacted every customer that
received the recalled meat. This level of verification checks is well above the
percentage of checks conducted by USDA district offices for the Class I recalls
we reviewed.
Appendix II
Federal Actions Associated with the Discovery of an Animal in the United
States Infected with BSE
Page 40 GAO-05-51 Food Recall Programs
On December 26, 2003, USDA began checking the primary and secondary
customers of the recalling company that it was aware of, although the entire
product distribution chain was unknown. During the checks, USDA tried to
determine if the product was further distributed, and it used verification
checks to acquire distribution lists for secondary and tertiary customers of the
recalling company.
Verification checks continued until February 25, 2004. Three USDA districts
conducted these verification checks. The Boulder District coordinated the checks
and assigned checks to the Minneapolis District Office for customers in Montana
and to the Alameda District Office for customers in California. USDA required
that 100 percent of the primary checks, 50 percent of the secondary checks, and
20 percent of the tertiary checks be conducted on-site. According to USDA, more
than 50 percent of the secondary checks were actually conducted on-site. FDA
officials helped conduct verification checks. According to USDA, the recall took
a long time to complete because USDA contacted each customer at least twice.
USDA first contacted each customer to conduct the check and again to verify
product disposition.
On February 25, 2004, the Boulder District concluded that the recall was
conducted in an effective manner. On March 1, 2004, USDA’s Recall Management
Division recommended that the agency terminate the recall, and USDA sent a
letter to the recalling company to document that USDA considered the recall to
be complete.
Recall Was Complicated by Inaccurate Distribution Lists and Mixing of
Potentially Contaminated and Noncontaminated Beef
USDA used distribution lists and shipping records to piece together where
the recalled product was distributed. According to USDA, one of the recalling
company’s three primary customers was slow in providing its customer list. USDA
could not begin verification activities for that primary customer without this
list. Furthermore, some customers of the recalling company provided USDA with
imprecise lists that did not specify which customers received the recalled
product. As a consequence, USDA could not quickly determine the scope of product
distribution and had to take time conducting extra research using shipping
invoices to determine which specific customers received the product.
Even when USDA determined the amount and location of beef, the agency still
had trouble tracking the beef in certain types of establishments, such as
grocery store distributors. USDA could not easily track the individual stores
where those distributors sent the beef because of product mixing
Appendix II
Federal Actions Associated with the Discovery of an Animal in the United
States Infected with BSE Page 41 GAO-05-51 Food Recall Programs
and the distributors’ record-keeping practices. Generally, distributors
purchase beef from multiple sources, mix it in their inventory, and lose track
of the source of the beef they send to the stores that they supply. To deal with
this problem, USDA first identified the dates when recalled beef was shipped to
the distributors and then asked for a list of the stores that were shipped any
beef after those dates. Consequently, some stores were included in the recall
that may never have received recalled beef.
The recall was also complicated by repeated mixing of recalled beef with
nonrecalled beef, thereby increasing the amount of meat involved in the recall.
The recalling company slaughtered 23 cows on December 9, 2003, and shipped those
and 20 other carcasses to a primary customer on December 10, 2003. The recalling
company’s carcasses were tagged to identify the slaughter date and the
individual cow. The primary customer removed the identification tags and mixed
the 23 recalled carcasses with the 20 nonrecalled carcasses. Because the
carcasses could not be distinguished, the recall included all 43 carcasses at
the primary customer. After one round of processing at the primary customer, the
meat from the carcasses was shipped to two other processing facilities. Both
establishments further mixed the recalled meat from the 43 carcasses with meat
from other sources. In all, the mixing of beef from 1 BSE-positive cow resulted
in over 500 customers receiving potentially contaminated beef. Imprecise
distribution lists and the mixing of recalled beef combined to complicate USDA’s
identification of where the product went. Specifically, on December 23, 2003,
USDA’s initial press release stated that the recalling company was located in
Washington State. Three days later, on December 26, 2003, USDA announced that
the recalled beef was distributed within Washington and Oregon. On December 27,
2003, USDA determined that one of the primary customers of the recalling firm
distributed beef to facilities in California and Nevada, in addition to
Washington and Oregon, for a total of four states. On December 28, 2003, USDA
announced that some of the secondary customers of the recalling company may also
have distributed the product to Alaska, Montana, Hawaii, Idaho, and Guam, for a
total of eight states and one territory.
On January 6, 2004, over 2 weeks from recall initiation, USDA determined
that the beef went to only six states—Washington, Oregon, California, Nevada,
Idaho, and Montana—and that no beef went to Alaska, Hawaii, or Guam. To reach
that conclusion, USDA used the distribution lists, shipping records, and sales
invoices that it received from companies to piece together exactly where the
recalled beef may have been sent. The lists
Appendix II
Federal Actions Associated with the Discovery of an Animal in the United
States Infected with BSE Page 42 GAO-05-51 Food Recall Programs
showed that 713 customers may have received the recalled beef; 6 of those
may have received beef from more than one source. USDA determined that 176
customers on the lists did not actually receive recalled beef, including the
customers in Guam and Hawaii. USDA’s review also indicated that recalled beef
was probably not shipped to Alaska or Utah, and USDA checked 2 retailers in
Alaska and 3 retailers in Utah to confirm that was the case. In total, USDA
conducted verification checks on 537 of the 713 customers on the lists. USDA’s
initial checks identified an additional 45 customers that may have received the
recalled beef that were not included on the distribution lists, for a total of
582 verification checks. Figure 4 summarizes USDA’s verification efforts during
the recall.
Appendix II
Federal Actions Associated with the Discovery of an Animal in the United
States Infected with BSE Page 43 GAO-05-51 Food Recall Programs
Figure 4: USDA’s Recall Verification Checks by Location and Customer Type
for Meat Associated with the Animal Infected with BSE
Note: USDA checked 15 primary, 40 secondary, and 526 tertiary customers
plus the recalling company, for a total of 582 verification checks. USDA’s press
release stated that the recall involved 10,410 pounds of beef products, and the
USDA recall coordinator for this recall told us that downstream processors mixed
the recalled beef with nonrecalled beef, for a total of more than 38,000 pounds
of beef that was distributed at the secondary customer level. According to USDA
officials involved with the
D = Distributor R = Retailer SF = Storage facility P = Processor Primary
customers (15 total) Recalling slaughterhouse (WA) 1 R (OR) 1 P (WA) 1 P (OR) 1
P (OR) 11 R (WA) Secondary customers (40 total) Tertiary customers (526 total) 1
R (OR) 1 SF (OR) 3 D (OR) 3 D (WA) 2 dual D (OR) 59 R (OR) 79 R (WA) 5 R (ID) 3
R (UT) 4 R (MT) 161 R (WA) 8 R (ID) 15 R (OR) 2 R (AK) 31 R (OR) 8 R (WA) 10 R
(NV) 5 R (ID) 10 R (CA) 2 R (CA) 17 R (OR) 5 R (WA) 1 D (NV) 11 R (CA) 85 R (NV)
3 D (OR) 11 R (OR) 2 D (CA) 26 R (CA) 2 R (WA)
( ) Acronyms in parentheses are postal abbreviations for each state.
Source: GAO analysis of USDA verification check documents.
Appendix II
Federal Actions Associated with the Discovery of an Animal in the United
States Infected with BSE
Page 44 GAO-05-51 Food Recall Programs
recall, the precise amount of meat that was sold at the retail level is
unknown because retailers at the tertiary level further mixed nonrecalled meat
with potentially contaminated meat. USDA told us that more than 64,000 pounds of
beef was ultimately returned or destroyed by customers, and that, because of the
mixing, it was not able to determine how much of the original 10,410 pounds of
recalled beef was contained in the 64,000 pounds that were recovered.
FDA’s Role in USDA’s Recall
Parts of the BSE-infected animal slaughtered on December 9, 2003, were not
used for food, but they were sent to renderers to be separated into raw
materials, such as proteins and blood. Rendered materials are used for many
purposes, including cosmetics and vaccines. FDA has jurisdiction over renderers.
When USDA learned of the BSE-infected cow on December 23, 2003, the agency
immediately notified FDA. On December 24, 2003, FDA sent an inspection team to a
renderer that handled materials from the BSE cow. Inspectors confirmed that the
parts of the slaughtered BSE positive cow were on the premises. FDA later
identified a second company that potentially rendered material from the
slaughtered BSE cow. Both renderers agreed to voluntarily hold all product
processed from the diseased cow and dispose of the product as directed by FDA
and local authorities.
On January 7, 2004, 15 containers of potentially contaminated, rendered
material (meat and bone meal) were inadvertently loaded on a ship, and on
January 8, 2004, the ship left Seattle, Washington, for Asia. The renderer
initiated steps to recover the shipped material, so it could be disposed of as
directed by FDA and local authorities. The ship carrying the material returned
to the United States on February 24, 2004, and the material was disposed of in a
landfill on March 2, 2004. On January 12, 2004, FDA asked both renderers to
expand their voluntary holds to rendered materials processed from December 23,
2003, through January 9, 2004, because they may have rendered some recalled meat
or trim that was recovered from retail establishments. Both renderers agreed to
the expanded product hold. In total, FDA requested that renderers voluntarily
hold approximately 2,000 tons of rendered material. FDA confirmed that none of
the potentially contaminated, rendered material entered commerce, because FDA
accounted for all rendered material. FDA
Appendix II
Federal Actions Associated with the Discovery of an Animal in the United
States Infected with BSE Page 45 GAO-05-51 Food Recall Programs
reported that no recall was necessary because no product was distributed
commercially by the rendering companies.
USDA and FDA Worked Together on the Recall USDA and FDA worked together in
two ways. First, both agencies notified each other if their investigations
yielded any information about products within the jurisdiction of the other
agency. For instance, when conducting the second round of verification checks,
USDA tracked the disposition of the product to renderers and landfills and
notified FDA when the product went to renderers. Second, FDA officials helped
conduct verification checks. FDA conducted 32 of the 582 verification checks
(approximately 5 percent) for the USDA recall. Officials from both agencies
indicated they regularly interacted and shared information. Table 3 outlines the
agencies’ actions.
Table 3: Detailed Timeline of USDA, FDA, and Company Actions Related to the
Discovery of an Animal Infected with BSE Date USDA recall actions FDA actions
Company actions 12/9/03 • USDA samples cow for BSE. • BSE cow is slaughtered.
12/11/03 • Sample is sent to Ames, Iowa, for BSE testing. • Recalling company
sends carcasses to primary customer for processing. 12/12/03 • Primary customer
sends meat products to two other primary customers for further processing. 12/12
- 12/23/03 • Other primary customers distribute recalled product to secondary
customers. • Secondary customers distribute recalled product to tertiary
customers. 12/23/03 • BSE test results are presumptively positive. • Recall
meeting. • Initiation of voluntary recall. • Press release. • FDA notified of
BSE test results. • FDA dispatches investigation teams. 12/24/03 • FDA inspects
Renderer 1. • FDA determines some rendered material from Renderer 1 is intended
for Indonesia. • FDA discovers some material may have been sent to Renderer 2. •
Renderer 1 agrees to hold remaining rendered material. • Recalling company
contacts primary customers. • Primary customers contact their customers.
Appendix II Federal Actions Associated with the Discovery of an Animal in the
United States Infected with BSE Page 46 GAO-05-51 Food Recall Programs 12/25/03
• USDA receives confirmation from reference lab in England that cow in question
is BSE positive. 12/26/03 • Verification checks begin • USDA announces recalled
product in Washington State and Oregon. • FDA begins process of comparing
records to ensure all products from Renderers 1 and 2 are accounted for. •
Renderer 2 agrees to hold all material that may have been derived from BSE cow.
None of the rendered material has been distributed. 12/27/03 • USDA announces
recalled product was distributed in Washington State, Oregon, California, and
Nevada. • FDA issues statement confirming that the rendering plants that
processed all of the nonedible material from the BSE cow have placed a voluntary
hold on all of the potentially infectious product, none of which had left the
control of the companies and entered commercial distribution. 12/28/03 • USDA
announces recalled product was distributed in Washington State, Oregon,
California, Nevada, Montana, Idaho, Alaska, Hawaii, and Guam. 12/29/03 • Food
Safety and Inspection Service determines that the recalled meat products were
distributed to 42 locations, with 80 percent of the products distributed to
stores in Oregon and Washington State. 12/31/03 • FDA offers assistance to USDA
to complete recall verification checks. 1/6/04 • USDA determines recalled
product was only distributed in Washington State, Oregon, California, Nevada,
Montana, and Idaho. 1/8/04 • FDA is notified by the renderer that some of the
rendered material on hold from Renderer 1 was inadvertently shipped to Asia.
Renderer 1 commits to isolate and return the rendered material. • Rendering
company notifies FDA of shipment of product on hold. (Continued From Previous
Page) Date USDA recall actions FDA actions Company actions Appendix II Federal
Actions Associated with the Discovery of an Animal in the United States Infected
with BSE Page 47 GAO-05-51 Food Recall Programs Source: GAO analysis of USDA and
FDA information. 1/12/04 • FDA advises Renderers 1 and 2 that they may have
rendered meat or trim subject to recall from retail stores. • FDA requests
Renderers 1 and 2 to place all rendered material from December 23 to January 9
on hold. • FDA determines neither renderer had shipped rendered material
manufactured after December 23, 2003. 2/9/04 • All rendered material was
disposed of in landfill, except material shipped to Asia. 2/24/04 • Ship
carrying rendered material returns to U.S. port. 2/25/04 • Verification checks
complete. • USDA Boulder District Office concludes recall is effective. 3/1/04 •
Recall is closed. 3/2/04 • FDA observes disposal in landfill of remaining
rendered material...
snip...
REPORTS
1. Food Safety: USDA and FDA Need to Better Ensure Prompt and Complete
Recalls of Potentially Unsafe Food. GAO-05-51, October 7.tss http://www.gao.gov/cgi-bin/getrpt?GAO-05-51
Highlights - http://www.gao.gov/highlights/d0551high.pdf
Texas
FDA Statement
FOR IMMEDIATE RELEASE Statement May 4, 2004
Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a
cow with central nervous system symptoms had been killed and shipped to a
processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began
an investigation. On Friday and throughout the weekend, FDA investigators
inspected the slaughterhouse, the rendering facility, the farm where the animal
came from, and the processor that initially received the cow from the
slaughterhouse.
FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over the
weekend FDA was able to track down all the implicated material. That material is
being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known as "mad
cow disease," can exhibit such symptoms. In this case, there is no way now to
test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit
the feeding of its rendered protein to other ruminant animals (e.g., cows,
goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing
the firm that FDA will not object to use of this material in swine feed only. If
it is not used in swine feed, this material will be destroyed. Pigs have been
shown not to be susceptible to BSE. If the firm agrees to use the material for
swine feed only, FDA will track the material all the way through the supply
chain from the processor to the farm to ensure that the feed is properly
monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian
protein out of animal feed for cattle and other ruminant animals. FDA
established its animal feed rule in 1997 after the BSE epidemic in the U.K.
showed that the disease spreads by feeding infected ruminant protein to
cattle.
Under the current regulation, the material from this Texas cow is not
allowed in feed for cattle or other ruminant animals. FDA's action specifying
that the material go only into swine feed means also that it will not be fed to
poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely
with the U.S. Department of Agriculture on all BSE issues. The animal feed rule
provides crucial protection against the spread of BSE, but it is only one of
several such firewalls. FDA will soon be improving the animal feed rule, to make
this strong system even stronger.
####
rule
Terry S. Singeltary Sr. wrote:
THAT ONE TEXAS MAD COW IS ONLY TIP OF ICE BURG;
No mad cow results for nearly 500 cows
By Steve Mitchell United Press International Published 8/11/2004 11:23 AM
WASHINGTON, Aug. 11 (UPI) -- The U.S. Department of Agriculture failed to
test for mad cow disease or collect the correct portion of the brain on nearly
500 suspect cows over the past two years -- including some in categories
considered most likely to be infected -- according to agency records obtained by
United Press International.
The testing problems mean it may never be known with certainty whether
these animals were infected with the deadly disease. Department officials said
these animals were not included in the agency's final tally of mad cow tests,
but the records, obtained by UPI under the Freedom of Information Act, indicate
at least some of them were counted...
snip...
--
Steve Mitchell is UPI's Medical Correspondent. E-mail sciencemail@upi.com
Copyright © 2001-2004 United Press International
HERE IS THE TEXAS MAD COW THAT WENT TO THE RENDER WITHOUT BEING TESTED AND
OTHER MULTIPLE FLAWS IN THE SYSTEM;
July 13, 2004
IG Audit Finds Multiple Flaws in Mad Cow Surveillance Plan Rep. Waxman
raises questions about the effectiveness and credibility of USDA's response to
mad cow disease, citing an audit by the USDA Inspector General that finds
systemic deficiencies in the Department's surveillance plan and new evidence
that USDA misled the public in the wake of the detection of an infected cow in
Washington State.
- Letter to USDA
IG Draft Audit
May 13, 2004
Failure To Test Staggering Cow May Reflect Wider Problems Rep. Waxman
raises concerns that the recent failure of USDA to test an impaired cow for BSE
may not be an isolated incident, citing the failure of USDA to monitor whether
cows condemned for central nervous system symptoms are actually tested for mad
cow disease.
- Letter to USDA
=============================================== TSS
BIO-RAD BSE TEST POLITICAL REPLY TO TSS
Subject: FSIS NOTICE SAMPLE COLLECTION FROM CATTLE UNDER THE BOVINE
SPONGIFORM ENCEPHALOPATHY (BSE) ONGOING SURVEILLANCE PROGRAM From: "Terry S.
Singeltary Sr." Reply-To: Sustainable Agriculture Network Discussion Group Date:
Fri, 2 Feb 2007 17:32:58 -0600
Subject: Re: USDA/APHIS JUNE 2004 'ENHANCED' BSE/TSE COVER UP UPDATE
DECEMBER 19, 2004 USA Date: Thu, 30 Dec 2004 12:27:06 -0600 From: "Terry S.
Singeltary Sr.
BSE-L
snip...
> > OH, i did ask Bio-Rad about this with NO reply to date; > >
> -------- Original Message --------
> Subject: USA BIO-RADs INCONCLUSIVEs
> Date: Fri, 17 Dec 2004 15:37:28 –0600
> From: "Terry S. Singeltary Sr."
> To: susan_berg@bio-rad.com
> > > > Hello Susan and Bio-Rad,
> > Happy Holidays!
> > I wish to ask a question about Bio-Rad and USDA BSE/TSE testing
> and there inconclusive. IS the Bio-Rad test for BSE/TSE that
complicated,
> or is there most likely some human error we are seeing here?
> > HOW can Japan have 2 positive cows with
> No clinical signs WB+, IHC-, HP- ,
> BUT in the USA, these cows are considered 'negative'?
> > IS there more politics working here than science in the USA?
> > What am I missing?
> > >
> -------- Original Message --------
> Subject: Re: USDA: More mad cow testing will demonstrate beef's safety
> Date: Fri, 17 Dec 2004 09:26:19 –0600
> From: "Terry S. Singeltary Sr." > snip...end > >
> Experts doubt USDA's mad cow results
snip...END
WELL, someone did call me from Bio-Rad about this, however it was not Susan
Berg. but i had to just about take a blood oath not to reveal there name. IN
fact they did not want me to even mention this, but i feel it is much much to
important. I have omitted any I.D. of this person, but thought I must document
this ;
Bio-Rad, TSS phone conversation 12/28/04
Finally spoke with ;
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph:
510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX
at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation
with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they
seem to keep having. X was very very cautious as to speak directly about USDA
and it's policy of not using WB. X was very concerned as a Bio-Rad official of
retaliation of some sort. X would only speak of what other countries do, and
that i should take that as an answer. I told X I understood that it was a very
loaded question and X agreed several times over and even said a political one.
my question;
Does Bio-Rad believe USDA's final determination of False positive, without
WB, and considering the new atypical TSEs not showing positive with -IHC and -HP
???
ask if i was a reporter. i said no, i was with CJD Watch and that i had
lost my mother to hvCJD. X did not want any of this recorded or repeated.
again, very nervous, will not answer directly about USDA for fear of
retaliation, but again said X tell me what other countries are doing and
finding, and that i should take it from there. "very difficult to answer"
"very political"
"very loaded question"
outside USA and Canada, they use many different confirmatory tech. in house
WB, SAF, along with IHC, HP, several times etc. you should see at several talks
meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE.
again, look what the rest of the world is doing. said something about Dr.
Houston stating; any screening assay, always a chance for human error. but with
so many errors (i am assuming X meant inconclusive), why are there no
investigations, just false positives? said something about ''just look at the
sheep that tested IHC- but were positive''. ...
TSS
-------- Original Message --------
Subject: Your questions
Date: Mon, 27 Dec 2004 15:58:11 –0800
From: To: flounder@wt.net
Hi Terry:
............................................snip
Let me know your phone number so I can talk to you about the Bio-Rad BSE
test. Thank you
Regards
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph:
510-741-6720 Fax: 510-741-5630 Email:
=================================
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
(see COPIOUS AMOUNTS OF mad cow feed in COMMERCE IN ALABAMA...TSS)
Texas BSE Investigation Final Epidemiology Report August 2005
State-Federal Team Responds to Texas BSE Case
JUNE 30, 2005
(please note 7+ month delay in final confirmation so the BSE MRR policy
could be set in stone first. $$$...tss)
*** SEE ATTEMPTED COVER-UP BEFORE THE END AROUND BY FONG ET AL OF THE O.I.G
The U.S. Department of Agriculture confirmed June 29 that genetic testing
had verified bovine spongiform encephalopathy (mad cow disease) in a 12-year-old
cow that was born and raised in a Texas beef cattle herd.
Subsequent epidemiological investigations resulted in the culling and
testing of 67 adult animals from the index herd. Bio-Rad tests for BSE were
conducted on all 67 animals by the National Veterinary Services Laboratory
(NVSL) in Ames, Iowa. All tests were negative.
On July 12, Texas officials lifted the quarantine on the source herd. At
press time, USDA's Animal and Plant Health Inspection Service was tracing
animals of the same age that had left the ranch.
Timeline
The BSE-positive animal was a Brahman-cross cow born and raised in a
single Texas herd. The location of the ranch was not disclosed.
On Nov. 11, 2004, the 12-year-old cow was taken to a Texas auction market.
Because of its condition, the cow was sent to Champion Pet Foods in Waco, Texas.
The company produces several blends of dog food, primarily for the greyhound
industry.
On Nov. 15, the animal arrived dead at Champion. Under procedures
established by USDA's intensive surveillance program, a sample was sent to the
USDA-approved Texas Veterinary Medical Diagnostic Testing Laboratory (TVMDL) at
Texas A&M University.
Between June 1, 2004, and June 1, 2005, TVMDL tested nearly 34,000 samples
from Texas, New Mexico, Arkansas and Louisiana. They tested the sample from
Champion on Nov. 19 using a Bio-Rad ELISA rapid test for BSE. Initial results
were inconclusive.
Because of the inconclusive results, a representative from USDA took the
entire carcass to TVMDL where it was incinerated. USDA's Animal and Plant Health
Inspection Service (APHIS) began tracing the animal and herd.
The sample was then sent to the National Veterinary Services Laboratory
for further testing. Two Immunohistochemistry (IHC) tests were conducted and
both were negative for BSE. At that point APHIS stopped their trace.
USDA scientists also ran an additional, experimental IHC "rapid" tissue
fixation test for academic purposes. This test has not been approved
internationally.
Some abnormalities were noted in the experimental test, but because the
two approved tests came back negative, the results were not reported beyond the
laboratory.
Monitoring by OIG
USDA's Office of Inspector General (OIG) has been monitoring
implementation of the BSE expanded surveillance program and evaluating the
following:
* Effectiveness of the surveillance program;
* Performance of BSE laboratories in complying with policies and
procedures for conducting tests and reporting results;
* Enforcement of the ban on specified risk materials in meat
products;
* Controls to prevent central nervous system tissue in advanced meat
recovery products;
* Ante mortem condemnation procedures; and
* Procedures for obtaining brain tissue samples from condemned
cattle.
While reviewing voluminous records, OIG auditors noticed conflicting test
results on one sample-rapid inconclusive, IHC negative, experimental
reactive.
Sample retested
At the recommendation of the Inspector General, the sample was retested
during the week of June 5 with a second confirmatory test, the Western Blot. The
results were reactive.
USDA scientists then conducted an additional IHC confirmatory test, using
different antibodies from the November 2004 test. On Friday, June 10, Secretary
of Agriculture Mike Johanns publicly announced the results as a "weak
positive."
On June 16 an official with USDA's National Veterinary Services Laboratory
hand-carried samples for further testing to the Veterinary Laboratory Agency
(VLA) in Weybridge, England. Since 1991, the VLA has been a BSE reference
laboratory for the World Organization for Animal Health (OIE).
Experts from the Weybridge lab confirmed the accuracy of the results of
USDA's November confirmatory IHC test, concurring that the case could not have
been confirmed on the basis of this sample. They also examined the November
experimental IHC test and interpreted the results to be positive.
Weybridge also conducted additional tests, including IHC, OIE-prescribed
Western Blot, NaTTA Western Blot and Prionics Western Blot tests.
To better understand the conflicting results, USDA also conducted Bio-Rad
and IDEXX rapid screening tests, IHC and OIE-prescribed Western Blot. USDA also
used DNA sequencing to determine the prion protein gene sequence of the
animal.
Texas even had a 'secret' test that showed that mad cow positive;
experimental IHC test results, because the test was not a validated procedure,
and because the two approved IHC tests came back negative, the results were not
considered to be of regulatory significance and therefore were not reported
beyond the laboratory. . A Western blot test conducted the week of June 5, 2005,
returned positive for BSE.
48 hr BSE confirmation turnaround took 7+ months to confirm this case, so
the BSE MRR policy could be put into place. ...TSS
*** -------- Original Message --------***
***Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov,
contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at
OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully
request a full inquiry into the cover-up of TSEs in the United States of America
over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff,
Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST
In Reply to:
Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding
further analysis of BSE Inconclusive Test Results
posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days
later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary
for Marketing and Regulatory Programs resigns. Three days later same mad cow
found in November turns out to be positive. Both resignation are unexpected.
just pondering... TSS
MAD COW IN TEXAS NOVEMBER 2004. ...TSS
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 -0600
From: "Terry S. Singeltary Sr."
To: Carla EverettReferences: [log in to unmask]; [log in to unmask]
;
Greetings Carla, still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food
chain?
and i see the TEXAS department of animal health is ramping up for
something, but they forgot a url for update?
I HAVE NO ACTUAL CONFIRMATION YET...
can you confirm??? terry
============================================================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr."References;[log in to unmask];
The USDA has made a statement, and we are referring all callers to the
USDA web site. We have no information about the animal being in Texas.
Carla
At 09:44 AM 11/19/2004, you wrote:
Greetings Carla,
i am getting unsubstantiated claims of this BSE 'inconclusive' cow is
from
TEXAS. can you comment on this either way please?
thank you,
Terry S. Singeltary Sr
======================================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr."References: <[log in to
unmask]><[log in to unmask] us><[log in to unmask]> <[log in
to unmask]us> <[log in to unmask]>
our computer department was working on a place holder we could post USDA's
announcement of any results. There are no results to be announced tonight by
NVSL, so we are back in a waiting mode and will post the USDA announcement when
we hear something.
At 06:05 PM 11/22/2004,
you wrote:
why was the announcement on your TAHC site removed?
Bovine Spongiform Encephalopathy:
November 22: Press Release title here
star image More BSE information
terry
Carla Everett wrote:
no confirmation on the U.S.'inconclusive test...
no confirmation on location of animal. ;
FROM HERE, IT TOOK 7 MONTHS TO CONFIRM THIS MAD COW, while the BSE MRR
policy was being bought and sold...(in my opinion...tss)
Saturday, August 16, 2008
Qualitative Analysis of BSE Risk Factors in the United States February 13,
2000 at 3:37 pm PST (BSE red book)
TEXAS OFFICIALS DEAD WRONG ON AMOUNT OF INFECTIVITY TO CAUSE A TSE PRION
DISEASE ;
"FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams – approximately a quarter ounce — of prohibited
material. These animals weigh approximately 600 pounds."
5.5 GRAMS OF INFECTIOUS PROHIBITED MAD COW FEED FOR EACH OF THE 1,222
ANIMALS (5.5 GRAMS X 1,222 ANIMALS) IS ENOUGH INFECTIOUS MAD COW FEED TO KILL A
SMALL HERD OF COWS...TSS
U.S. Food and Drug Administration FDA News | Today the Food and Drug
Administ…U.S. Food and Drug Administration FDA News
Today the Food and Drug Administration announced the results of tests
taken on feed used at a Texas feedlot that was suspected of containing meat and
bone meal from other domestic cattle — a violation of FDA’s 1997 prohibition on
using ruminant material in feed for other ruminants. Results indicate that a
very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams – approximately a quarter ounce — of prohibited
material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in
origin (therefore not likely to contain infected material because there is no
evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even if the
feed were contaminated.
According to Dr. Bernard Schwetz, FDA’s Acting Principal Deputy
Commissioner, “The challenge to regulators and industry is to keep this disease
out of the United States. One important defense is to prohibit the use of any
ruminant animal materials in feed for other ruminant animals. Combined with
other steps, like U.S. Department of Agriculture’s (USDA) ban on the importation
of live ruminant animals from affected countries, these steps represent a series
of protections, to keep American cattle free of BSE.”
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing
that it is voluntarily purchasing all 1,222 of the animals held in Texas and
mistakenly fed the animal feed containing the prohibited material. Therefore,
meat from those animals will not enter the human food supply. FDA believes any
cattle that did not consume feed containing the prohibited material are
unaffected by this incident, and should be handled in the beef supply clearance
process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting
the human error that resulted in the misformulation of the animal feed
supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into
place is essential for protecting the food supply and that continued vigilance
needs to be taken, by all concerned, to ensure these rules are followed
routinely.
FDA will continue working with USDA as well as State and local officials
to ensure that companies and individuals comply with all laws and regulations
designed to protect the U.S. food supply.
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242
Consumer Inquiries: 888-INFO-FDA
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests
taken on feed used at a Texas feedlot that was suspected of containing meat and
bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on
using ruminant material in feed for other ruminants. Results indicate that a
very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams - approximately a quarter ounce -- of prohibited
material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in
origin (therefore not likely to contain infected material because there is no
evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even if the
feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy
Commissioner, "The challenge to regulators and industry is to keep this disease
out of the United States. One important defense is to prohibit the use of any
ruminant animal materials in feed for other ruminant animals. Combined with
other steps, like U.S. Department of Agriculture's (USDA) ban on the importation
of live ruminant animals from affected countries, these steps represent a series
of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless
announcing that it is voluntarily purchasing all 1,222 of the animals held in
Texas and mistakenly fed the animal feed containing the prohibited material.
Therefore, meat from those animals will not enter the human food supply. FDA
believes any cattle that did not consume feed containing the prohibited material
are unaffected by this incident, and should be handled in the beef supply
clearance process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting
the human error that resulted in the misformulation of the animal feed
supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into
place is essential for protecting the food supply and that continued vigilance
needs to be taken, by all concerned, to ensure these rules are followed
routinely.
FDA will continue working with USDA as well as State and local officials
to ensure that companies and individuals comply with all laws and regulations
designed to protect the U.S. food supply.
PRION 2009 CONGRESS BOOK OF ABSTRACTS
O.4.3
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after
oral transmission
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard
Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera
and Vaccines, Germany; 2Department of Neuropathology, Georg-August University,
Göttingen, Germany, 3Department of Virology and Immunology, German Primate
Centre, Göttingen, Germany
Background: BSE-infected cynomolgus monkeys represent a relevant animal
model to study the pathogenesis of variant Creutzfeldt-Jacob disease
(vCJD).
Objectives: To study the spread of BSE prions during the asymptomatic
phase of infection in a simian animal model.
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time
points during the incubation period and 7 orally BSE-dosed macaques were
sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues
were tested for the presence of proteinase-K-resistant prion protein (PrPres) by
western immunoblot and by paraffin-embedded tissue (PET) blot technique.
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres
deposits were widely spread in neuronal tissues (including the peripheral
sympathetic and parasympathetic nervous system) and in lymphoid tissues
including tonsils. In asymptomatic disease carriers, PrPres deposits could be
detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were
negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and
medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas
sympathetic trunk and all thoracic/cervical segments of the spinal cord were
still negative for PrPres. However, tonsil samples were negative in all
asymptomatic cases.
Discussion: There is evidence for an early spread of BSE to the CNS via
autonomic fibres of the splanchnic and vagus nerves indicating that
trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils
were predominantly negative during the main part of the incubation period
indicating that epidemiological vCJD screening results based on the detection of
PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of
vCJD among humans.
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral
Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3;
Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6;
Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique,
France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious
Disease control, Sweden; 5Georg August University, Germany; 6German Primate
Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans
to contract BSE through contaminated food. For this purpose, BSE brain was
titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose
(MID50) for oral exposure to BSE in a simian model, and, by in doing this, to
assess the risk for humans. Secondly, we aimed at examining the course of the
disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of
BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study,
animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005
mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already
developed simian vCJD upon oral or intracerebral exposure or are at the onset of
the clinical phase. However, there are differences in the clinical course
between orally and intracerebrally infected animals that may influence the
detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral
route using less than 5 g BSE brain homogenate. The difference in the incubation
period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years).
However, there are rapid progressors among orally dosed monkeys that develop
simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfillment of the study “BSE
in primates“ supported by the EU (QLK1-2002-01096).
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral
route using less than 5 g BSE brain homogenate.
look at the table and you'll see that as little as 1 mg (or 0.001 gm)
caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in
primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to non-human
primates. We gave two macaques a 5 g oral dose of brain homogenate from a
BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months
after exposure, whereas the other remained free of disease at 76 months. On the
basis of these findings and data from other studies, we made a preliminary
estimate of the food exposure risk for man, which provides additional assurance
that existing public health measures can prevent transmission of BSE to
man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15
(7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a similar
PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of disease in
the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic
ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula
Published online January 27, 2005
Calves were challenged by mouth with homogenised brain from confirmed
cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They
were then left to develop BSE, but were not subjected to the normal stresses
that they might have encountered in a dairy herd. Animals in all four groups
developed BSE. There has been a considerable spread of incubation period in some
of the groups, but it appears as if those in the 1 and 10g challenge groups most
closely fit the picture of incubation periods seen in the epidemic. Experiments
in progress indicate that oral infection can occur in some animals with doses as
low as 0.01g and 0.001g. .........
It is clear that the designing scientists must also have shared Mr
Bradley's surprise at the results because all the dose levels right down to 1
gram triggered infection.
6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100 grams) was probably given with the benefit of hindsight;
particularly if one considers that later in the same answer Mr Bradley expresses
his surprise that it could take as little of 1 gram of brain to cause BSE by the
oral route within the same species. This information did not become available
until the "attack rate" experiment had been completed in 1995/96. This was a
titration experiment designed to ascertain the infective dose. A range of
dosages was used to ensure that the actual result was within both a lower and an
upper limit within the study and the designing scientists would not have
expected all the dose levels to trigger infection. The dose ranges chosen by the
most informed scientists at that time ranged from 1 gram to three times one
hundred grams. It is clear that the designing scientists must have also shared
Mr Bradley's surprise at the results because all the dose levels right down to 1
gram triggered infection.
FULL 130 LASHINGS TO USDA BY OIG again
FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms On Friday,
April 30 th , the Food and Drug Administration learned that a cow with central
nervous system symptoms had been killed and shipped to a processor for rendering
into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began
an investigation. On Friday and throughout the weekend, FDA investigators
inspected the slaughterhouse, the rendering facility, the farm where the animal
came from, and the processor that initially received the cow from the
slaughterhouse.
FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over the
weekend FDA was able to track down all the implicated material. That material is
being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known as "mad
cow disease," can exhibit such symptoms. In this case, there is no way now to
test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit
the feeding of its rendered protein to other ruminant animals (e.g., cows,
goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing
the firm that FDA will not object to use of this material in swine feed only. If
it is not used in swine feed, this material will be destroyed. Pigs have been
shown not to be susceptible to BSE. If the firm agrees to use the material for
swine feed only, FDA will track the material all the way through the supply
chain from the processor to the farm to ensure that the feed is properly
monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian
protein out of animal feed for cattle and other ruminant animals. FDA
established its animal feed rule in 1997 after the BSE epidemic in the U.K.
showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not
allowed in feed for cattle or other ruminant animals. FDA's action specifying
that the material go only into swine feed means also that it will not be fed to
poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely
with the U.S. Department of Agriculture on all BSE issues. The animal feed rule
provides crucial protection against the spread of BSE, but it is only one of
several such firewalls. FDA will soon be improving the animal feed rule, to make
this strong system even stronger.
####
*** 2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006 ***
ALABAMA MAD COW CASE
CJDIBSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific
Advisors and Consultants Staff January 2001 Meeting (short version)
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,2001 3:03 PM freas ...
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
2015
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
It is clear that the designing scientists must also have shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
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. ...
10 years post mad cow feed ban August 1997
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
16 years post mad cow feed ban August 1997
2013
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
17 years post mad cow feed ban August 1997
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain
Specified Risk Materials BSE TSE Prion
*** Monday, October 26, 2015 ***
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015 ***
the OIE BSE TSE Prion policy now, the BSE MRR, legalized the free trading
of the TSE Prion disease, humans and animals have now become expendable.
...
‘’AS i said before, OIE should hang up there jock strap now, since it
appears they will buckle every time a country makes some political hay about
trade protocol, commodities and futures. IF they are not going to be science
based, they should do everyone a favor and dissolve there organization.’’
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to the Central Bureau,
snip...see ;
Sunday, October 18, 2015
World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
Thursday, December 17, 2015
Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738
10 December 2015
Friday, January 1, 2016
South Korea Lifts Ban on Beef, Veal Imports From Canada
US CONGRESS, another failed entity...tss
Tuesday, December 29, 2015
*** Congress repeals country-of-origin labeling rule for beef and pork
December 28, 2015 at 2:21am
*** Australian government assessing risk of importing beef from US, Japan
and the Netherlands
Thursday, December 24, 2015
Infectious disease spread is fueled by international trade
*** you can find some history of the BSE cases in Canada and Klein’s BSE
SSS policy comment here ;
Tuesday, August 12, 2014
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST
2014
Saturday, December 12, 2015
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
*** Needless conflict ***
Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b
Published online 16 May 2012
Terry S. Singeltary Sr. said:
I kindly wish to submit the following please ;
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary:
The transmissible spongiform encephalopathies (also called prion diseases)
are fatal neurodegenerative diseases that affect animals and humans. The agent
of prion diseases is a misfolded form of the prion protein that is resistant to
breakdown by the host cells. Since all mammals express prion protein on the
surface of various cells such as neurons, all mammals are, in theory, capable of
replicating prion diseases. One example of a prion disease, bovine spongiform
encephalopathy (BSE; also called mad cow disease), has been shown to infect
cattle, sheep, exotic undulates, cats, non-human primates, and humans when the
new host is exposed to feeds or foods contaminated with the disease agent. The
purpose of this study was to test whether non-human primates (cynomologous
macaque) are susceptible to the agent of sheep scrapie. After an incubation
period of approximately 10 years a macaque developed progressive clinical signs
suggestive of neurologic disease. Upon postmortem examination and microscopic
examination of tissues, there was a widespread distribution of lesions
consistent with a transmissible spongiform encephalopathy. This information will
have a scientific impact since it is the first study that demonstrates the
transmission of scrapie to a non-human primate with a close genetic relationship
to humans. This information is especially useful to regulatory officials and
those involved with risk assessment of the potential transmission of animal
prion diseases to humans.
Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion
disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the
past decades, c-BSE's zoonotic potential has been the driving force in
establishing extensive protective measures for animal and human health. In
complement to the recent demonstration that humanized mice are susceptible to
scrapie, we report here the first observation of direct transmission of a
natural classical scrapie isolate to a macaque after a 10-year incubation
period. Neuropathologic examination revealed all of the features of a prion
disease: spongiform change, neuronal loss, and accumulation of PrPres throughout
the CNS.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats
SUMMARY: We are reopening the comment period for our proposed rule that
would revise completely the scrapie regulations, which concern the risk groups
and categories established for individual animals and for flocks, the use of
genetic testing as a means of assigning risk levels to animals, movement
restrictions for animals found to be genetically less susceptible or resistant
to scrapie, and recordkeeping requirements. This action will allow interested
persons additional time to prepare and submit comments.
DATES: The comment period for the proposed rule published on September 10,
2015 (80 FR 54660-54692) is reopened. We will consider all comments that we
receive on or before December 9, 2015. ...
COMMENT SUBMISSION TERRY S. SINGELTARY SR.
WITH regards to Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats, I
kindly submit the following ;
>>>The last major revision of the scrapie regulations occurred on
August 21, 2001, when we published in theFederal Register(66 FR 43964, Docket
No. 97-093-5) a final rule amending part 79 by imposing additional restrictions
on the interstate movement of sheep and goats.<<<
Indeed, much science has changed about the Scrapie TSE prion, including
more science linking Scrapie to humans. sadly, politics, industry, and trade,
have not changed, and those usually trump sound science, as is the case with all
Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing
animals and the OIE. we can look no further at the legal trading of the Scrapie
TSE prion both typical and atypical of all strains, and CWD all stains. With as
much science of old, and now more new science to back this up, Scrapie of all
types i.e. atypical and typical, BSE all strains, and CWD all strains, should be
regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE,
and all trading partners to take heed to the latest science on the TSE prion
disease, all of them, and seriously reconsider the blatant disregards for human
and animal health, all in the name of trade, with the continued relaxing of TSE
Prion trade regulations through the ‘NEGLIGIBLE BSE RISK’ PROGRAM, which was set
up to fail in the first place. If the world does not go back to the ‘BSE RISK
ASSESSMENTS’, enhance, and or change that assessment process to include all TSE
prion disease, i.e. ‘TSE RISK ASSESSMENT’, if we do not do this and if we
continue this farce with OIE and the USDA et al, and the ‘NEGLIGIBLE BSE RISK’
PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they
will continue to mutate and spread among species of human and animal origin, and
they will continue to kill. ...
please see ;
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
snip...see ;
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS
COMMISSION Paris, 19–28 February 2013
In response to a Member Country’s detailed justification for listing of
chronic wasting disease of cervids (CWD) against the criteria of Article 1.2.2.,
the Code Commission recommended this disease be reconsidered for listing.
CWD TO HUMANS RISK FACTORS STILL IGNORED
REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS
COMMISSION Paris, 17–26 September 2013
Item 5 Criteria for listing diseases (Chapter 1.2.)
Comments were received from Australia, EU, Japan, New Zealand, Switzerland,
Thailand and AU-IBAR The Code Commission noted a Member Country’s comment
suggesting that greater clarity was needed for the term ‘significant morbidity
and mortality’. As noted in the February 2013 report, the Code Commission
considered that the structured process of listing diseases, first by an expert
group whose conclusions are documented and circulated for Member Countries’
review and comment, then consideration by the World Assembly of Delegates before
final adoption, is sufficiently rigorous and transparent.
link updated ;
Monday, May 05, 2014
Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing
*** Singeltary submission ;
*** Program Standards: Chronic Wasting Disease Herd Certification Program
and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
*** DOCUMENT ID: APHIS-2006-0118-0411 ***
see attachments PDF @ bottom of submission...tss
SCRAPIE TO HUMANS RISK FACTORS STILL IGNORED
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
98 | Veterinary Record | January 24, 2015
EDITORIAL
Scrapie: a particularly persistent pathogen
Cristina Acín
Resistant prions in the environment have been the sword of Damocles for
scrapie control and eradication. Attempts to establish which physical and
chemical agents could be applied to inactivate or moderate scrapie infectivity
were initiated in the 1960s and 1970s,with the first study of this type focusing
on the effect of heat treatment in reducing prion infectivity (Hunter and
Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate
the prion protein are based on the method developed by Kimberlin and
collaborators (1983). This procedure consists of treatment with 20,000 parts per
million free chlorine solution, for a minimum of one hour, of all surfaces that
need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so
on). Despite this, veterinarians and farmers may still ask a range of questions,
such as ‘Is there an official procedure published somewhere?’ and ‘Is there an
international organisation which recommends and defines the exact method of
scrapie decontamination that must be applied?’
From a European perspective, it is difficult to find a treatment that could
be applied, especially in relation to the disinfection of surfaces in lambing
pens of affected flocks. A 999/2001 EU regulation on controlling spongiform
encephalopathies (European Parliament and Council 2001) did not specify a
particular decontamination measure to be used when an outbreak of scrapie is
diagnosed. There is only a brief recommendation in Annex VII concerning the
control and eradication of transmissible spongiform encephalopathies (TSE
s).
Chapter B of the regulation explains the measures that must be applied if
new caprine animals are to be introduced to a holding where a scrapie outbreak
has previously been diagnosed. In that case, the statement indicates that
caprine animals can be introduced ‘provided that a cleaning and disinfection of
all animal housing on the premises has been carried out following
destocking’.
Issues around cleaning and disinfection are common in prion prevention
recommendations, but relevant authorities, veterinarians and farmers may have
difficulties in finding the specific protocol which applies. The European Food
and Safety Authority (EFSA ) published a detailed report about the efficacy of
certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and
even a formulation of copper or iron metal ions in combination with hydrogen
peroxide, against prions (EFSA 2009). The report was based on scientific
evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006,
Solassol and others 2006) but unfortunately the decontamination measures were
not assessed under outbreak conditions.
The EFSA Panel on Biological Hazards recently published its conclusions on
the scrapie situation in the EU after 10 years of monitoring and control of the
disease in sheep and goats (EFSA 2014), and one of the most interesting findings
was the Icelandic experience regarding the effect of disinfection in scrapie
control. The Icelandic plan consisted of: culling scrapie-affected sheep or the
whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of
stables, sheds, barns and equipment with high pressure washing followed by
cleaning with 500 parts per million of hypochlorite; drying and treatment with
300 ppm of iodophor; and restocking was not permitted for at least two years.
Even when all of these measures were implemented, scrapie recurred on several
farms, indicating that the infectious agent survived for years in the
environment, even as many as 16 years after restocking (Georgsson and others
2006).
In the rest of the countries considered in the EFSA (2014) report,
recommendations for disinfection measures were not specifically defined at the
government level. In the report, the only recommendation that is made for sheep
is repopulation with sheep with scrapie-resistant genotypes. This reduces the
risk of scrapie recurrence but it is difficult to know its effect on the
infection.
Until the EFSA was established (in May 2003), scientific opinions about TSE
s were provided by the Scientific Steering Committee (SSC) of the EC, whose
advice regarding inactivation procedures focused on treating animal waste at
high temperatures (150°C for three hours) and high pressure alkaline hydrolysis
(SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory
Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe
working and the prevention of TSE infection. Annex C of the ACDP report
established that sodium hypochlorite was considered to be effective, but only if
20,000 ppm of available chlorine was present for at least one hour, which has
practical limitations such as the release of chlorine gas, corrosion,
incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its
active chemicals and the stability of dilutions (ACDP 2009).
In an international context, the World Organisation for Animal Health (OIE)
does not recommend a specific disinfection protocol for prion agents in its
Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General
recommendations on disinfection and disinsection (OIE 2014), focuses on
foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on
prion disinfection. Nevertheless, the last update published by the OIE on bovine
spongiform encephalopathy (OIE 2012) indicates that few effective
decontamination techniques are available to inactivate the agent on surfaces,
and recommends the removal of all organic material and the use of sodium
hydroxide, or a sodium hypochlorite solution containing 2 per cent available
chlorine, for more than one hour at 20ºC.
The World Health Organization outlines guidelines for the control of TSE s,
and also emphasises the importance of mechanically cleaning surfaces before
disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO
1999).
Finally, the relevant agencies in both Canada and the USA suggest that the
best treatments for surfaces potentially contaminated with prions are sodium
hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution,
while most commercial household bleaches contain 5.25 per cent sodium
hypochlorite. It is therefore recommended to dilute one part 5.25 per cent
bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency
2013).
So what should we do about disinfection against prions? First, it is
suggested that a single protocol be created by international authorities to
homogenise inactivation procedures and enable their application in all
scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available
chlorine seems to be the procedure used in most countries, as noted in a paper
summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015).
But are we totally sure of its effectiveness as a preventive measure in a
scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease
be needed?
What we can conclude is that, if we want to fight prion diseases, and
specifically classical scrapie, we must focus on the accuracy of diagnosis,
monitoring and surveillance; appropriate animal identification and control of
movements; and, in the end, have homogeneous and suitable protocols to
decontaminate and disinfect lambing barns, sheds and equipment available to
veterinarians and farmers. Finally, further investigations into the resistance
of prion proteins in the diversity of environmental surfaces are required.
References
snip...
98 | Veterinary Record | January 24, 2015
*** These results suggest that AA fibrils are relatively heat stable and
that similar to prions, autoclaving at 135 °C is required to destroy the
pathogenicity of AA fibrils.
*** These findings may contribute to the prevention of AA fibril
transmission through food materials to different animals and especially to
humans.
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Monday, January 4, 2016
Long live the OIE, or time to close the doors on a failed entity?
Saturday, December 12, 2015
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS STILL
DON'T GET IT $
Chronic Wasting Unease
The emergence of a deadly disease has wildlife officials and deer breeders
eyeing each other suspiciously.
Subject: Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using
Population Monitoring and Capture-Recapture Data
To date, we are unaware of a study that documents a decrease in CWD
prevalence over time in mule deer, white-tailed deer or elk. We briefly consider
three plausible explanations for our findings: a) that natural oscillations
occur in CWD outbreaks; b) that the outbreak has peaked and is declining to a
lower endemic level; or c) that previous management actions were more successful
at suppressing the outbreak than originally believed.
Sharp & Pastor [41] illustrated that CWD outbreaks may play out as a
series of reoccurring epidemics characterized by either stable limit cycles or
oscillations that may dampen or amplify as a function of deer density. If this
is the case, we would expect today’s declining deer population to feedback on
conditions–lowering transmission rates leading to reduced CWD effects and a
growing population. Increasing abundance would support higher transmission
rates, deer decline, and oscillations of CWD prevalence and deer. Alternatively,
Almberg et al. [21] (see also [22–24,41,42]) suggested that CWD outbreaks could
reach endemic equilibrium characterized by coexistence of a smaller deer
population and CWD. Under these scenarios, population prevalence would reach a
lower, constant level after a period of high prevalence and deer decline.
Although neither of the foregoing scenarios can be dismissed completely,
invoking them ignores the extensive management of this deer population that
occurred in the years between the two time points we chose as the basis for our
analyses. Management aimed to reduce CWD transmission between 2000 and 2005,
which included a combination of (crude and unpopular) focal culling and a
broader increase in female harvest, decreased overall deer abundance by about
25%. Analyses carried out shortly after suggested that reductions in deer
density had made little impact on CWD prevalence [10]. However, our current
findings suggest that these management actions may indeed have attenuated the
outbreak. Observed dynamics over the last decade closely approximate those
predicted from models by Wild et al. [42] that included a substantial amount of
selective predation on CWD-infected individuals. That harvest could be a source
of selective mortality is supported by an early notion that CWD-infected deer
might be more vulnerable to harvest [43], just as infected deer also appear to
be more vulnerable to vehicle collisions and predation [20,33,44]. This offers
the possibility that hunting could be used as a more tightly controlled
substitute for predation in studies of system responses with CWD and perhaps
other similar diseases.
The protracted time-scale of the CWD outbreak is much longer than the
timespan of our research, which limits our ability to identify the true
explanation of our findings. Nonetheless, our research suggests that, at least
for the foreseeable future (e.g., decades), mule deer populations sharing the
overall survival and infection probabilities estimated from our analyses may
persist but likely will not thrive where CWD becomes established as an endemic
infectious disease.
‘’Nonetheless, our research suggests that, at least for the foreseeable
future (e.g., decades), mule deer populations sharing the overall survival and
infection probabilities estimated from our analyses may persist but likely will
not thrive where CWD becomes established as an endemic infectious disease. ‘’
*** Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using
Population Monitoring and Capture-Recapture Data
‘’Mountain lions prey selectively on CWD infected deer [33] and CWD could
result in an abundance of vulnerable prey, thereby enhancing mountain lion
survival and reproduction [20].’’
please see ;
‘’preliminary results suggesting that bobcats (Lynx rufus) may be
susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting
disease agent.’’
references on Feline Spongiform Encephalopathy FSE toward the bottom, see
;
Assessing Transmissible Spongiform Encephalopathy Species Barriers with an
In Vitro Prion Protein Conversion Assay
Friday, January 01, 2016
Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population
Monitoring and Capture-Recapture Data
Saturday, December 12, 2015
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
Wednesday, December 30, 2015
Michigan Deer suspected positive for CWD found in Watertown Township; Jan.
12 public meeting set
http://chronic-wasting-disease.blogspot.com/2015/12/michigan-deer-suspected-positive-for.html
Tuesday, December 29, 2015
TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS STILL
DON'T GET IT $
Chronic Wasting Unease
The emergence of a deadly disease has wildlife officials and deer breeders
eyeing each other suspiciously.
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
MOM
Thursday, December 24, 2015
Revisiting the Heidenhain Variant of Creutzfeldt-Jakob Disease: Evidence
for Prion Type Variability Influencing Clinical Course and Laboratory Findings
Article type: Research Article
Evidence for human transmission of amyloid-β pathology and cerebral amyloid
angiopathy
07 02:27 AM
Terry S. Singeltary Sr. said:
re-Evidence for human transmission of amyloid-? pathology and cerebral
amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26
April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated
online 11 September 2015 Erratum (October, 2015)
*** I would kindly like to comment on the Nature Paper, the Lancet reply,
and the newspaper articles.
snip...see full text ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO
PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report them in
their proper context. 'This hopefully will avoid misunderstanding and possible
distortion by the media to portray the results as having more greater
significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the researchers have demonstrated the transmission of a pathological process
from two cases one of severe Alzheimer's disease the other of
Gerstmann-Straussler disease to marmosets. However they have not demonstrated
the transmission of either clinical condition as the "animals were behaving
normally when killed". As the report emphasises the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see if the conditions, as
opposed to the partial pathological process, is transmissible.
what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of
things highly unusual. However it could be argued that the results reveal a
potential risk, in that brain tissue from these two patients has been shown to
transmit a pathological process. Should therefore brain tissue from such cases
be regarded as potentially infective? Pathologists, morticians, neuro surgeons
and those assisting at neuro surgical procedures and others coming into contact
with "raw" human brain tissue could in theory be at risk. However, on a priori
grounds given the highly specific route of transmission in these experiments
that risk must be negligible if the usual precautions for handling brain tissue
are observed.
1
92/11.4/1.1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required’’ before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Terry S. Singeltary Sr.
P.S.
Thursday, January 14, 2016
Terry S. Singeltary Sr.
P.S.
ANIMAL HEALTH REPORT 2006 (BSE h-BASE ALABAMA) BLOG URL CHANGE
Wednesday, March 26, 2008
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or
Italian L-BASE
Thursday, January 3, 2008
ANIMAL HEALTH REPORT 2006 (BSE h-BASE EVENT IN ALABAMA, Scrapie, and CWD)
*** NEW URL STARTING HERE ;
EMERGING ANIMAL DISEASES Actions Needed to Better Position USDA to Address
Future Risks Report to the Chairman, Committee on Energy and Commerce, House of
Representatives December 2015 GAO-16-132
GAO
Terry S. Singeltary Sr.
