Susceptibility of European Red Deer (Cervus elaphus elaphus) to Alimentary
Challenge with Bovine Spongiform Encephalopathy
Mark P. Dagleish , * E-mail: mark.dagleish@moredun.ac.uk
Affiliation: Moredun Research Institute, Pentlands Science Park, Bush Loan,
Penicuik, Near Edinburgh EH26 0PZ, United Kingdom
⨯ Stuart Martin, Affiliation: Animal Health & Veterinary Laboratories
Agency Lasswade, Pentlands Science Park, Bush Loan, Penicuik, Near Edinburgh
EH26 0PZ, United Kingdom
⨯ Philip Steele, Affiliation: Moredun Research Institute, Pentlands Science
Park, Bush Loan, Penicuik, Near Edinburgh EH26 0PZ, United Kingdom
⨯ Jeanie Finlayson, Affiliation: Moredun Research Institute, Pentlands
Science Park, Bush Loan, Penicuik, Near Edinburgh EH26 0PZ, United Kingdom
⨯ Samantha L. Eaton, Affiliation: Neurobiology Division, The Roslin
Institute at, Royal (Dick) School of Veterinary Studies, University of
Edinburgh, Easter Bush Campus, Midlothian, EH25 9RG, United Kingdom
⨯ Sílvia Sisó, Affiliation: Animal Health & Veterinary Laboratories
Agency Lasswade, Pentlands Science Park, Bush Loan, Penicuik, Near Edinburgh
EH26 0PZ, United Kingdom
⨯ Paula Stewart, Affiliation: Neurobiology Division, The Roslin Institute
at, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter
Bush Campus, Midlothian, EH25 9RG, United Kingdom
⨯ Natalia Fernández-Borges, Affiliation: CIC bioGUNE, Parque tecnológico de
Bizkaia, Derio 48160, Spain
⨯ Scott Hamilton, Affiliation: Moredun Research Institute, Pentlands
Science Park, Bush Loan, Penicuik, Near Edinburgh EH26 0PZ, United Kingdom
⨯ Yvonne Pang, Affiliation: Moredun Research Institute, Pentlands Science
Park, Bush Loan, Penicuik, Near Edinburgh EH26 0PZ, United Kingdom
⨯ Francesca Chianini, Affiliation: Moredun Research Institute, Pentlands
Science Park, Bush Loan, Penicuik, Near Edinburgh EH26 0PZ, United Kingdom
⨯ Hugh W. Reid, Affiliation: Moredun Research Institute, Pentlands Science
Park, Bush Loan, Penicuik, Near Edinburgh EH26 0PZ, United Kingdom
⨯ Wilfred Goldmann, Affiliation: Neurobiology Division, The Roslin
Institute at, Royal (Dick) School of Veterinary Studies, University of
Edinburgh, Easter Bush Campus, Midlothian, EH25 9RG, United Kingdom
⨯ Lorenzo González, Affiliation: Animal Health & Veterinary
Laboratories Agency Lasswade, Pentlands Science Park, Bush Loan, Penicuik, Near
Edinburgh EH26 0PZ, United Kingdom
⨯ Joaquín Castilla, Affiliations: CIC bioGUNE, Parque tecnológico de
Bizkaia, Derio 48160, Spain, IKERBASQUE, Basque Foundation for Science, Bilbao
48013, Bizkaia, Spain
⨯ [ ... ], Martin Jeffrey Affiliation: Animal Health & Veterinary
Laboratories Agency Lasswade, Pentlands Science Park, Bush Loan, Penicuik, Near
Edinburgh EH26 0PZ, United Kingdom
⨯ [ view all ] [ view less ] Susceptibility of European Red Deer (Cervus
elaphus elaphus) to Alimentary Challenge with Bovine Spongiform Encephalopathy
Mark P. Dagleish, Stuart Martin, Philip Steele, Jeanie Finlayson, Samantha L.
Eaton, Sílvia Sisó, Paula Stewart, Natalia Fernández-Borges, … Scott Hamilton,
Yvonne Pang PLOS x Published: January 23, 2015 DOI: 10.1371/journal.pone.0116094
Abstract
European red deer (Cervus elaphus elaphus) are susceptible to the agent of
bovine spongiform encephalopathy, one of the transmissible spongiform
encephalopathies, when challenged intracerebrally but their susceptibility to
alimentary challenge, the presumed natural route of transmission, is unknown. To
determine this, eighteen deer were challenged via stomach tube with a large dose
of the bovine spongiform encephalopathy agent and clinical signs, gross and
histological lesions, presence and distribution of abnormal prion protein and
the attack rate recorded. Only a single animal developed clinical disease, and
this was acute with both neurological and respiratory signs, at 1726 days post
challenge although there was significant (27.6%) weight loss in the preceding
141 days. The clinically affected animal had histological lesions of vacuolation
in the neuronal perikaryon and neuropil, typical of transmissible spongiform
encephalopathies. Abnormal prion protein, the diagnostic marker of transmissible
encephalopathies, was primarily restricted to the central and peripheral nervous
systems although a very small amount was present in tingible body macrophages in
the lymphoid patches of the caecum and colon. Serial protein misfolding cyclical
amplification, an in vitro ultra-sensitive diagnostic technique, was positive
for neurological tissue from the single clinically diseased deer. All other
alimentary challenged deer failed to develop clinical disease and were negative
for all other investigations. These findings show that transmission of bovine
spongiform encephalopathy to European red deer via the alimentary route is
possible but the transmission rate is low. Additionally, when deer carcases are
subjected to the same regulations that ruminants in Europe with respect to the
removal of specified offal from the human food chain, the zoonotic risk of
bovine spongiform encephalopathy, the cause of variant Creutzfeldt-Jakob
disease, from consumption of venison is probably very low.
snip...
Discussion
This investigation resulted in the first and only known case, to
date, of clinical disease or accumulation of abnormal PrPd in any cervid species
due to oral challenge with BSE. The increase in incubation period compared to
European red deer challenged with BSE intra-cerebrally (1060 days) [33] compared
to oral challenge (1727 days) is approximately 60% and similar to the
differences observed in incubation periods for sheep or goats when challenged
with TSE agents by these two routes [40,41]. The neurological clinical signs
observed could be broadly related to the spongiform encephalopathy and the
accumulation of PrPd in that the restlessness, stereotypic head movements and
pacing may be due to compromise of the nucleus accumbens [42], found in the
striatum, and the laboured breathing due to the lesions in the medulla, where
the respiratory centre is located [43]. Alternatively, the laboured and audible
mouth breathing may have been due to, or contributed to by, compromise of either
of the recurrent laryngeal nerves resulting in some degree of laryngeal
paralysis but we were unable to determine this. Apart from the gradual loss of
body weight, the speed of onset of clinical signs and progression was very rapid
but animal welfare requirements precluded any further longitudinal study of
these. The clinical signs described for this animal are broadly similar to those
reported for clinical BSE in European red deer challenged via the intracerebral
route [33], clinical cases of CWD in deer [44] and clinical cases of BSE in
cattle [45].
snip...see full text ;
MANY THANKS TO THE AUTHORS FOR THEIR WORK ON THE TSE PRION DISEASE, AND TO
THEM AND PLOS FOR OPEN ACCESS, THANK YOU!...TSS
2008-05-28
***Therefore, although BSE has never been diagnosed in any deer species, a
possible risk to human health remains via ingestion of cervine products. Chronic
wasting disease (CWD), also a TSE, naturally infects several cervid species in
North America and is spreading rapidly in both captive and free-ranging
populations.
Conclusions: This study shows that deer are susceptible to BSE by
intracerebral inoculation and display clinical signs and vacuolar pathology that
are similar to those of CWD. ***These findings highlight the importance of
preventing the spread to Europe of CWD from North America as this may
necessitate even more extensive testing of animal tissues destined for human
consumption within the EU.
***Although the absence of PrPd in lymphoid and other non-neurological
tissues potentially limits the risk of transmission to humans, the replication
of TSE agents in peripheral tissues following intra-cerebral challenge is often
limited. Thus the assessment of risk posed by cervine BSE as a human pathogen or
for environmental contamination should await the outcome of ongoing oral
challenge experiments.
2008-05-28
From: TSS
Subject: EXPERIMENTAL TRANSMISSION OF BSE TO EUROPEAN RED DEER
Date: May 29, 2008 at 11:30 am PST
Experimental transmission of bovine spongiform encephalopathy to European
red deer (Cervus elaphus elaphus)
Bovine spongiform encephalopathy (BSE), a member of the transmissible
spongiform encephalopathies (TSE), primarily affects cattle. Transmission is via
concentrate feed rations contaminated with infected meat and bone meal
(MBM).
In addition to cattle, other food animal species are susceptible to BSE and
also pose a potential threat to human health as consumption of infected meat
products is the cause of variant Creutzfeldt-Jakob disease in humans, which is
invariably fatal. In the UK, farmed and free ranging deer were almost certainly
exposed to BSE infected MBM in proprietary feeds prior to legislation banning
its inclusion.
***Therefore, although BSE has never been diagnosed in any deer species, a
possible risk to human health remains via ingestion of cervine products. Chronic
wasting disease (CWD), also a TSE, naturally infects several cervid species in
North America and is spreading rapidly in both captive and free-ranging
populations.
Results: Here we show that European red deer (Cervus elaphus elaphus) are
susceptible to intra-cerebral (i/c) challenge with BSE positive cattle brain
pool material resulting in clinical neurological disease and weight loss by
794-1290 days and the clinical signs are indistinguishable to those reported in
deer with CWD.
Spongiform changes typical of TSE infections were present in brain and
accumulation of the disease-associated abnormal prion protein (PrPd) was present
in the central and peripheral nervous systems, but not in lymphoid or other
tissues. Western immunoblot analysis of brain material showed a similar
glycosylation pattern to that of BSE derived from infected cattle and
experimentally infected sheep with respect to protease-resistant PrP
isoforms.
However, the di-, mono- and unglycosylated bands migrated significantly (p
<0 .001="" affected="" and="" brains="" bse="" cattle="" clinically="" compared="" deer="" div="" from="" further="" in="" infected="" of="" samples="" sheep.="" the="" to="" when="">
Friday, December 14, 2012
Conclusions: This study shows that deer are susceptible to BSE by
intracerebral inoculation and display clinical signs and vacuolar pathology that
are similar to those of CWD. ***These findings highlight the importance of
preventing the spread to Europe of CWD from North America as this may
necessitate even more extensive testing of animal tissues destined for human
consumption within the EU.
***Although the absence of PrPd in lymphoid and other non-neurological
tissues potentially limits the risk of transmission to humans, the replication
of TSE agents in peripheral tissues following intra-cerebral challenge is often
limited. Thus the assessment of risk posed by cervine BSE as a human pathogen or
for environmental contamination should await the outcome of ongoing oral
challenge experiments.
Author: Mark P Dagleish, Stuart Martin, Philip Steele, Jeanie Finlayson,
Silvia Siso, Scott Hamilton, Francesca Chianini, Hugh W Reid, Lorenzo Gonzalez
and Martin Jeffrey Credits/Source: BMC Veterinary Research 2008, 4:17
Published on: 2008-05-28
FDA WARNING LETTER (14-ATL-04) adulterated under Section 402(a)(4) [21
U.S.C. 342(a)(4)] of the Act, protein derived from mammalian tissues to feeds
that may be used for ruminants [21 C.F.R. 589.2000(e)(1)(iii)(B)]
Newberry Feed & Farm, Inc. 2/14/14 Department of Health and Human
Services logoDepartment of Health and Human Services Public Health Service
Food and Drug Administration Atlanta District Office 60 8th St., NE
Atlanta, GA 30309
February 14, 2014
VIA UPS
J. Clint Layne, President/Co-owner Rhett Baker,
Secretary-Treasurer/Co-owner Newberry Feed & Farm Center, Inc. 131 Giff
Street Newberry, SC 29108
WARNING LETTER (14-ATL-04)
Dear Messrs. Layne and Baker,
An inspection of your feed mill located at 2431 Vincent Street, Newberry,
SC 29108 conducted by Investigators from the U.S. Food & Drug Administration
(FDA) and South Carolina Department of Agriculture on September 5-9, 2013
revealed significant violations of Current Good Manufacturing Practice (CGMP)
regulations for Medicated Feeds found in Title 21, Code of Federal Regulations,
Part 225 (21 C.F.R. 225). Such violations cause the medicated feeds manufactured
at your facility to be adulterated within the meaning of Section 501(a)(2)(B) of
the Federal Food, Drug, and Cosmetic Act (the Act) [21 U.S.C. § 351(a)(2)(B)] in
that the methods used in, or the facilities or controls used for the
manufacture, processing, packing, or holding of the medicated feeds do not
conform to or are not operated or administered in conformity with current good
manufacturing practices.
The inspection also revealed significant violations of the requirements set
forth in Title 21, Code of Federal Regulations, Section 589.2000 (21 C.F.R.
589.2000), Animal Proteins Prohibited in Ruminant Feed. This regulation is
intended to prevent the establishment and amplification of Bovine Spongiform
Encephalopathy (BSE). Animal feeds and feed ingredients containing prohibited
mammalian proteins are considered potentially injurious to ruminant and public
health. Because you failed to comply with the requirements set forth in 21
C.F.R. 589.2000, the feed products manufactured and distributed by your facility
are adulterated within the meaning of Section 402(a)(4) of the Act [21 U.S.C.
342(a)(4)] in that they have been prepared, packed, or held under insanitary
conditions whereby they may have become contaminated with filth or rendered
injurious to health. The adulterated feed was subsequently misbranded within the
meaning of Section 403(a)(1) of the Act [21 U.S.C. 343(a)(1)] because it was not
properly labeled with the required BSE cautionary statement.
Medicated Feed CGMP violations observed during the inspection include, but
are not limited to, the following:
1. You failed to ensure that all equipment that comes in contact with the
active drug component, feeds in process or finished medicated feed is subject to
reasonable and effective procedures to prevent unsafe contamination of feeds
with drugs. [21 C.F.R. 225.65(b)]
Your written equipment cleaning procedure that requires flushing with a
minimum of (b)(4) does not appear to be effective to prevent unsafe
contamination of your manufactured feed. During the inspection, our
Investigators observed a build-up of feed residue on surfaces inside the mixer
that was approximately three inches thick in accumulation. This build-up was
observed on the equipment throughout the inspection, including after flushing
had been performed. In addition, the cleaning procedure does not include
cleaning of the hand-add chute or scoops/buckets used to handle ingredients that
are then used to manufacture medicated feed. During the inspection, our
Investigators observed a build-up of feed residues approximately four inches
thick on the inside of the chute used to add the drug ingredients and other
“hand-adds”. Considering the extent of residue accumulation—some of which would
include the drug sources used in your medicated feeds—on surfaces in the mixer
and the hand-add chute, it is likely that chunks of this material break off
periodically, and may sometimes end up in feeds not intended to contain that
drug.
This is a repeat observation from the July 24-26, 2012 inspection. Your
response to the Form FDA 483, Inspectional Observations, issued to you following
the 2012 inspection stated the buckets and scoops would be replaced, and you
would schedule a regular cleaning of the equipment every (b)(4). Based on the
accumulation of residual feed observed on manufacturing equipment during the
inspection and which remained following flushing, you have either failed to
implement the promised corrective action or you have failed to ensure that the
corrective action was lasting and effective in preventing the violation from
recurring.
On October 3, 2013, we received your response to the Form FDA 483 issued to
you following the September 2013 inspection. You state in your response that you
have posted signs, added cleaning of the dump chute to the (b)(4) cleaning
procedure, and increased the physical cleaning of the mixer to (b)(4). You also
state that dedicated scoops will be used for each component or drug and have
ordered disposable liners for the buckets that will be discarded following each
dumping of product. However, you did not provide any documentation to
demonstrate these changes have been made, such as photos of the new sign or
newly cleaned equipment, or copies of the revised cleaning procedure.
2. You failed to investigate and implement corrective action where the
results of assays indicated that the level of drug in medicated feed was not in
accord with label specifications or not within permissible assay limits. An
original or copy of the record of such action must be maintained on the
premises. [21 C.F.R. 225.58(d)]
Your firm failed to adequately investigate and implement corrective action
when you received an assay result on 6/21/13 for a Type C medicated feed
containing Amprolium, showing the drug present at 73% of the concentration
stated on the label. This assay result is outside of the assay limits of 80-120%
established in 21 C.F.R. 558.4. The subsequent review of production and
inventory records conducted by your firm revealed these records were “OK”, and
it was determined the feed sample was taken incorrectly. Your firm’s
“\investigation sheet” dated 6/21/13 states the corrective action as “[t]rying
to make sure the samples are taken correctly.” No technique or procedural
changes were made in response to the described corrective action, however. Thus,
your firm failed to implement any corrective action in response to the out of
specification assay result.
Your firm also received assay results for a Type C medicated broiler feed
containing a Salinomycin concentration of 75% on 7/7/12 and 78% on 8/3/12. These
assay results are outside the specification tolerance of 80-120% of the
concentration stated on the label. [21 C.F.R. 558.4]. Your firm did not initiate
any investigation or corrective action after receiving these results. Failure to
investigate and implement corrective action following an out-of-limits assay is
a repeat observation from the July 24-26, 2012 inspection.
In your response to the Form FDA 483 issued to you following the September
2013 inspection, you state that you have instructed personnel further on
completing the investigation form and have also added sampling instructions to
the procedures manual. However, you did not provide copies of the new/revised
investigation form or the revisions to the procedures manual discussing
sampling.
3. Your daily inventory records fail to record the batches or production
runs (or lots) of medicated feed in which each drug was used. [21 C.F.R.
225.42(b)(6)(iii)] Although your daily inventory records appear to contain all
of the other required information, due to the way the form is designed, there is
only space to record one batch per day per drug and no space to record the name
of the product, lot number, or other identifier for that batch. Your daily
inventory record must reflect every batch or lot of medicated feed manufactured
each day.
4. You failed to document in the daily inventory record actions taken to
reconcile any discrepancies in the daily inventory record. [21 C.F.R.
225.42(b)(6)(v)] For example, the drug inventory conducted on 8/30/13 revealed a
discrepancy with respect to one fifty pound bag of (b)(4)(a Type A medicated
article). It does not appear that your firm took any action to reconcile this
discrepancy.
You state in your response to both #3 and #4 above that you have added an
area to the inventory control sheet to report any drugs that do not reconcile,
and that there is a space to make notes and/or adjustments to inventory to
ensure they reconcile. However, you did not indicate that the inventory control
sheet had been adjusted to provide for the possibility that any single drug may
be used more than once a day, and you did not provide any documentation—such as
a copy of the revised form—to demonstrate that these changes have been made.
5. You have failed to properly identify, store, handle, and control drugs
in your mixing areas to maintain their integrity and identity [21 C.F.R.
225.42(b)(4)]. Our inspection found that your firm was storing bags of Type A
Medicated Articles in a manner and location that allowed them to be covered in
bird droppings.
This finding also relates to your obligations under 21 C.F.R. 225.20(b)(2)
and (3), which requires the facility to be maintained in a reasonably clean and
orderly manner, and for access by birds and other pests to be minimized. During
the September 5-6, 2013 inspection, our Investigators observed birds (greater
than ten) nesting, flying, perched and foraging in the mill. Your response
indicated that you are investigating ways to keep birds out of the mill, but
that you did not yet have a plan at that time. You indicated that you would have
a plan in place by November 1, 2013, but did not provide further information
regarding any plan.
In addition, the following violations of the Animal Proteins Prohibited in
Ruminant Feed regulation [21 C.F.R. 589.2000] were observed during the
inspection:
1. You failed to use clean out procedures or other means adequate to
prevent carryover of protein derived from mammalian tissues to feeds that may be
used for ruminants [21 C.F.R. 589.2000(e)(1)(iii)(B)]. Your feed is therefore
adulterated under Section 402(a)(4) [21 U.S.C. 342(a)(4)] of the Act.
Because your firm uses animal proteins prohibited from use in ruminant
feeds, and also makes feeds for ruminants, you are required to have a cleanout
procedure adequate to prevent carryover into ruminant feeds. As noted above, our
Investigators observed a significant build-up of feed residues inside the feed
mixer and the hand-add chute, which remained following your cleanout procedure.
This equipment is used for processing both proteins derived from mammalian
tissues and feeds for ruminants. Since flushing was ineffective in removing the
accumulated feed from the equipment, your clean out procedure was inadequate to
prevent carryover of protein derived from mammalian tissues to feeds intended
for ruminant animals.
Your response indicates that your corrective actions for this item are the
same as for Item 1 above. However, as noted above, you did not provide any
documentation to demonstrate that the changes you discussed have been made, or
that they were adequate to address this issue.
2. You failed to label all products which contained or may have contained
prohibited materials and that are intended for use in animal feed with the BSE
cautionary statement, "Do not feed to cattle or other ruminants." [21 C.F.R.
589.2000(e)(1)(i).]
As discussed above, your clean out procedure is inadequate to prevent
carryover of protein derived from mammalian tissues to feeds intended for
ruminant animals. Thus, all feeds manufactured using your mixer and hand-add
chute that did not contain the BSE cautionary statement “Do not feed to cattle
or other ruminants,” are misbranded under Section 403(a)(1) [21 U.S.C.
343(a)(1)] of the Act. For example, a batch of Carolina Choice Beef Conditioner
Custom Mix (b)(4), manufactured on September 6, 2013, while there was a
significant build-up of feed residues in the feed mixer, was misbranded as its
label did not contain the required BSE cautionary statement.
The above is not intended to be an all-inclusive list of violations at your
facility. As a medicated and non-medicated feed manufacturer, you are
responsible for assuring that your overall operation and the products you
manufacture and distribute are in compliance with the law. You should take
prompt action to correct these violations, and you should establish procedures
whereby such violations do not recur. Failure to promptly correct these
violations may result in regulatory and/or administrative sanctions. These
sanctions include, but are not limited to, seizure, injunction, and/or notice of
opportunity for a hearing on a proposal to withdraw approval of your Medicated
Feed Mill License under Section 512(m)(4)(B)(ii) of the Act and 21 C.F.R.
515.22(c)(2).
Based on the results of the September 5-9, 2013 inspection, evaluated
together with the evidence before FDA when the Medicated Feed Mill License was
approved, the methods used in, or the facilities and controls used for, the
manufacture, processing, and packing of medicated feeds are inadequate to assure
and preserve the identity, strength, quality, and purity of the new animal drugs
therein. This letter constitutes official notification under the law and
provides you an opportunity to correct the above described violations.
You should notify this office, in writing, within fifteen (15) working days
of the receipt of this letter of the steps you have taken to bring your firm
into compliance with the law. Your response should include an explanation of
each step being taken to correct the violations and prevent their recurrence. In
your response, please include the timeframe in which the corrections will be
completed and provide any documentation that will effectively assist us in
evaluating whether the corrective actions have been made and the adequacy of
such. If you are unable to complete the corrective actions within fifteen (15)
working days, identify the reason for the delay and the time within which you
will complete the corrections. Include copies of any available documentation
demonstrating that corrections have been made.
Your written response should be sent to the U.S. Food and Drug
Administration, Attn: Janice L. King, Compliance Officer, at the address noted
in the letterhead. If you have questions, please contact Mrs. King at
843-746-2990 or write her at the noted address.
Sincerely, /S/ Philip S. Campbell Acting District Director Atlanta District
Office
cc: South Carolina Department of Agriculture, Phillip C. Trefsgar
HOLY MAD COW BATMAN, how much went out into commerce, how much was
recovered, what species are consuming these adulterated under Section 402(a)(4)
[21 U.S.C. 342(a)(4)] of the Act, protein derived from mammalian tissues to
feeds that may be used for ruminants [21 C.F.R. 589.2000(e)(1)(iii)(B)] ???
1. You failed to use clean out procedures or other means adequate to
prevent carryover of protein derived from mammalian tissues to feeds that may be
used for ruminants [21 C.F.R. 589.2000(e)(1)(iii)(B)]. Your feed is therefore
adulterated under Section 402(a)(4) [21 U.S.C. 342(a)(4)] of the Act.
Because your firm uses animal proteins prohibited from use in ruminant
feeds, and also makes feeds for ruminants, you are required to have a cleanout
procedure adequate to prevent carryover into ruminant feeds. As noted above, our
Investigators observed a significant build-up of feed residues inside the feed
mixer and the hand-add chute, which remained following your cleanout procedure.
This equipment is used for processing both proteins derived from mammalian
tissues and feeds for ruminants. Since flushing was ineffective in removing the
accumulated feed from the equipment, your clean out procedure was inadequate to
prevent carryover of protein derived from mammalian tissues to feeds intended
for ruminant animals.
Your response indicates that your corrective actions for this item are the
same as for Item 1 above. However, as noted above, you did not provide any
documentation to demonstrate that the changes you discussed have been made, or
that they were adequate to address this issue.
2. You failed to label all products which contained or may have contained
prohibited materials and that are intended for use in animal feed with the BSE
cautionary statement, "Do not feed to cattle or other ruminants." [21 C.F.R.
589.2000(e)(1)(i).]
As discussed above, your clean out procedure is inadequate to prevent
carryover of protein derived from mammalian tissues to feeds intended for
ruminant animals. Thus, all feeds manufactured using your mixer and hand-add
chute that did not contain the BSE cautionary statement “Do not feed to cattle
or other ruminants,” are misbranded under Section 403(a)(1) [21 U.S.C.
343(a)(1)] of the Act. For example, a batch of Carolina Choice Beef Conditioner
Custom Mix (b)(4), manufactured on September 6, 2013, while there was a
significant build-up of feed residues in the feed mixer, was misbranded as its
label did not contain the required BSE cautionary statement...end...TSS
Rocky Ford Pet Foods 8/27/13
Department of Health and Human Services logoDepartment of Health and Human
Services Public Health Service
Food and Drug Administration
Denver District Office
Bldg. 20-Denver Federal Center
P.O. Box 25087
6th Avenue & Kipling Street
Denver, Colorado 80225-0087
Telephone: 303-236-3000
FAX: 303-236-3100
August 27, 2013
WARNING LETTER
VIA UPS Overnight
Mr. Juan Manuel Villegas
Owner
Rocky Ford Pet Foods
21693 Highway 50 East
Rocky Ford, CO 81067
Ref. #: DEN-13-20-WL
Dear Mr. Villegas:
On February 25-27, 2013, the U.S. Food and Drug Administration (FDA)
conducted an inspection of your rendering facility located at 21693 Highway 50
East, Rocky Ford, Colorado. This inspection revealed significant deviations from
the requirements set forth in FDA regulations intended to reduce the risk of
bovine spongiform encephalopathy (BSE) within the United States. These
regulations are found in Title 21 of the Code of Federal Regulations (CFR),
Section 589.2000 (21 CFR 589.2000), Animal Proteins Prohibited in Ruminant Feed,
and Section 589.2001 (21 CFR 589.2001), Cattle Materials Prohibited in Animal
Food or Feed to Prevent the Transmission of Bovine Spongiform Encephalopathy.
These regulations address how renderers process (1) mammalian proteins
prohibited from use in ruminant food or feed and (2) materials designated as
“cattle materials prohibited in animal food or feed” (CMPAF) which are
prohibited from use in animal food or feed. CMPAF include, but are not limited
to:
The brain and spinal cord of cattle 30 months of age or older;
The entire carcass of cattle infected with BSE; and
The entire carcass of cattle 30 months of age or older that have not been
inspected and passed for human consumption if the brains and spinal cords were
not removed or otherwise effectively excluded from animal feed.
Your facility processes CMPAF.
Your failure to follow certain requirements of these regulations, as
described below, resulted in products manufactured and distributed by your
facilities being adulterated within the meaning of Section 402(a)(4) of the
Federal Food, Drug, and Cosmetic Act (the Act), [21 U.S.C. 342(a)(4)] and
misbranded within the meaning of Section 403(f) of the Act, [21 U.S.C. 343(f)].
You can find the Act, and its implementing regulations on the Internet through
links on the FDA’s web page at www.fda.gov1.
Our inspection revealed the following serious deviations from the
regulations at your rendering facility:
Failure to prevent the inclusion of cattle materials prohibited in animal
feed (CMPAF) in animal feed or feed ingredients, as required by 21 CFR
589.2001(c)(1). Specifically, on February 25, 2013, our investigator observed
that the unmarked CMPAF posterior sections of vertebral columns for two cows,
identified by your firm as older than 30 months of age, were separated from the
rest of the marked CMPAF material from those animals. The unmarked CMPAF
material was then commingled with 18 additional posterior vertebral columns and
placed in a trailer for shipment to another renderer for further processing and
possible use in animal feed.
You removed all 20 posterior vertebral columns from the trailer during the
inspection and stated that you would dispose of them in a landfill.
Failure to maintain adequate written procedures specifying how the process
of removing the brain and spinal cord from cattle not inspected and passed for
human consumption or 30 months of age or older is carried out, as required by 21
CFR 589.2001(c)(2)(ii). Specifically, your written procedure “Rocky Ford Ped
[sic] Food Standard Operating Procedure for handling 30 month and older Beef and
CMPAF Products” indicates that the head, vertebral column, and rib cage for
cattle 30 months of age and older are kept in one piece. This written procedure
is not consistent with actual operations observed at your firm on February 26,
2013. Our investigator observed that posterior vertebral columns from two cows
30 months of age or older were separated from the animals’ heads and anterior
vertebral columns; the posterior sections were not marked as CMPAF material.
Your written procedures fail to specify how, for animals 30 months of age or
older, posterior vertebral columns separated from marked anterior vertebral
columns would themselves be marked as CMPAF material.
Failure to mark the CMPAF and products that contain or may contain CMPAF
with an agent that can be readily detected on visual inspection, as required by
21 CFR 589.2001(c)(2)(v). Specifically, the posterior sections of vertebra
columns from cattle identified by your firm as 30 months of age or older were
separated from the head and anterior vertebral columns but then were not
identified as CMPAF with an agent readily detectable on visual examination.
Therefore, the CMPAF posterior vertebral columns were indistinguishable from the
non-CMPAF posterior vertebral columns.
Failure to label containers, including vehicles when used as containers,
which contain CMPAF with the required statement, “Do not feed to animals,” as
required by 21 CFR 589.2001(c)(2)(iv). Specifically, the dump truck and trailer
used for storage and transport of CMPAF materials did not bear the statement “Do
not feed to animals.”
Failure to avoid cross-contamination once CMPAF have been separated from
other cattle materials as required by 21 CFR 589.2001(c)(2)(iii). Specifically,
both marked and unmarked CMPAF were observed to be stored on the floor of the
processing area rather than in separate containers that adequately prevent
contact with animal feed, animal feed ingredients, or equipment surfaces, 21 CFR
589.2001(c)(2)(iii)(B). As described in item #1 above, the unmarked materials
were indistinguishable from non-CMPAF materials and could result in
cross-contamination.
This letter is not intended to serve as an all-inclusive list of violations
at your facility. As a manufacturer of materials intended for animal feed use,
you are responsible for ensuring your overall operation and the products you
manufacture and distribute are in compliance with the law. You should take
prompt action to correct these violations, and you should establish a system
whereby violations do not recur. Failure to promptly correct these violations
may result in regulatory action, such as seizure and/or injunction, without
further notice.
You should notify this office in writing of the steps you have taken to
bring your firm into compliance with the law within fifteen (15) working days of
receiving this letter. Your response should include each step that has been
taken or will be taken to correct the violations and prevent their recurrence.
If corrective action cannot be completed within fifteen (15) working days, state
the reason for the delay and the timeframe within which the corrections will be
completed. Please include copies of supporting documentation demonstrating that
corrections have been made.
Your written response should be sent to: U.S. Food and Drug Administration,
P.O. Box 25087, 6th Ave. and Kipling St., DFC, Bldg 20, Denver, CO 80225-0087,
Attn: Sarah A. Della Fave, Compliance Officer. If you have any questions about
this letter, please contact Ms. Della Fave at (303) 236-3006.
Sincerely,
/S/
LaTonya Mitchell
District Director
cc: Ronald K. Jones, D.V.M.
Denver District Manager
USDA/FSIS
PO Box 25387
DFC, Bldg 45
Denver, CO 80225
Laurel Hamling
Colorado Department of Agriculture
Feed Program
2331 W. 31st Avenue
Denver, CO 80211
-
Close Out Letter
Rocky Ford Pet Foods - Close Out Letter 4/16/142
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. *** This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada. *** It also
suggests a similar cause or source for atypical BSE in these countries. ***
see page 176 of 201 pages...tss
*** Singeltary reply ;
Molecular, Biochemical and Genetic Characteristics of BSE in Canada
*** Singeltary reply ;
31 Jan 2015 at 20:14 GMT
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s 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.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
==================================
In the USA, under the Food and Drug Administration’s 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.
=================================
Draft Guidance on Use of Material From Deer and Elk in Animal Feed; CVM
Updates on Deer and Elk Withdrawn FDA Veterinarian Newsletter July/August 2003
Volume XVIII, No 4
FDA has announced the availability of a draft guidance for industry
entitled “Use of Material from Deer and Elk in Animal Feed.” This draft guidance
document (GFI #158), when finalized, will describe FDA’s current thinking
regarding the use in animal feed of material from deer and elk that are positive
for Chronic Wasting Disease (CWD) or that are at high risk for CWD.
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the cervidae animal family (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer, white-tailed deer, North American elk, and farmed
black-tailed deer. CWD belongs to a family of animal and human diseases called
transmissible spongiform encephalopathies (TSEs). TSEs are very rare, but are
always fatal.
This draft Level 1 guidance, when finalized, will represent the Agency’s
current thinking on the topic. It does not create or confer any rights for or on
any person and does not operate to bind FDA or the public. An alternate method
may be used as long as it satisfies the requirements of applicable statutes and
regulations.
Draft guidance #158 is posted on the FDA/Center for Veterinary Medicine
Home Page. Single copies of the draft guidance may be obtained from the FDA
Veterinarian.
- - Page Last Updated: 04/16/2013
CONTAINS NON-BINDING RECOMMENDATIONS
158
Guidance for Industry
Use of Material from Deer and Elk in Animal Feed
Comments and suggestions regarding the document should be submitted to
Division of Dockets Management (HFA-305), Food and Drug Administration, 5630
Fishers Lane, Rm. 1061, Rockville, MD 20852. Submit electronic comments to http://www.regulations.gov. All comments
should be identified with the Docket No. 03D-0186.
For questions regarding this guidance, contact Burt Pritchett, Center for
Veterinary Medicine (HFV- 222), Food and Drug Administration, 7519 Standish
Place, Rockville, MD 20855, 240-453-6860, E-mail: burt.pritchett@fda.hhs.gov.
Additional copies of this guidance document may be requested from the
Communications Staff (HFV-12), Center for Veterinary Medicine, Food and Drug
Administration, 7519 Standish Place, Rockville, MD 20855, and may be viewed on
the Internet at http://www.fda.gov/AnimalVeterinary/GuidanceComplianceEnforcement/GuidanceforIndustry/default.htm.
U.S. Department of Health and Human Services
Food and Drug Administration Center for Veterinary Medicine September 15,
2003
CONTAINS NON-BINDING RECOMMENDATIONS
158
Guidance for Industry1
Use of Material from Deer and Elk in Animal Feed
This guidance represents the Food and Drug Administration’s current
thinking on the use of material from deer and elk in animal feed. It does not
create or confer any rights for or on any person and does not operate to bind
FDA or the public. You can use an alternative approach if the approach satisfies
the requirements of applicable statutes or regulations. If you want to discuss
an alternative approach, contact the FDA staff responsible for implementing this
guidance. If you cannot identify the appropriate FDA staff, call the appropriate
number listed on the title page of this guidance.
I. Introduction
FDA’s guidance documents, including this guidance, do not establish legally
enforceable responsibilities. Instead, guidances describe the Agency’s current
thinking on a topic and should be viewed only as recommendations, unless
specific regulatory or statutory requirements are cited. The use of the word
“should” in Agency guidances means that something is suggested or recommended,
but not required.
Under FDA’s BSE feed regulation (21 CFR 589.2000) most material from deer
and elk is prohibited for use in feed for ruminant animals. This guidance
document describes FDA’s recommendations regarding the use in all animal feed of
all material from deer and elk that are positive for Chronic Wasting Disease
(CWD) or are considered at high risk for CWD. The potential risks from CWD to
humans or non-cervid animals such as poultry and swine are not well understood.
However, because of recent recognition that CWD is spreading rapidly in
white-tailed deer, and because CWD’s route of transmission is poorly understood,
FDA is making recommendations regarding the use in animal feed of rendered
materials from deer and elk that are CWD-positive or that are at high risk for
CWD.
II. Background
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the animal family cervidae (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer,
1 This guidance has been prepared by the Division of Animal Feeds in the
Center for Veterinary Medicine (CVM) at the Food and Drug Administration.
1
CONTAINS NON-BINDING RECOMMENDATIONS
2
white-tailed deer, North American elk, and in farmed black-tailed deer. CWD
belongs to a family of animal and human diseases called transmissible spongiform
encephalopathies (TSEs). These include bovine spongiform encephalopathy (BSE or
“mad cow” disease) in cattle; scrapie in sheep and goats; and classical and
variant Creutzfeldt-Jakob diseases (CJD and vCJD) in humans. There is no known
treatment for these diseases, and there is no vaccine to prevent them. In
addition, although validated postmortem diagnostic tests are available, there
are no validated diagnostic tests for CWD that can be used to test for the
disease in live animals.
III.
Use in animal feed of material from CWD-positive deer and elk
Material from CWD-positive animals may not be used in any animal feed or
feed ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and
Cosmetic Act, animal feed and feed ingredients containing material from a
CWD-positive animal would be considered adulterated. FDA recommends that any
such adulterated feed or feed ingredients be recalled or otherwise removed from
the marketplace.
IV.
Use in animal feed of material from deer and elk considered at high risk
for CWD
Deer and elk considered at high risk for CWD include: (1) animals from
areas declared by State officials to be endemic for CWD and/or to be CWD
eradication zones; and (2) deer and elk that at some time during the 60-month
period immediately before the time of slaughter were in a captive herd that
contained a CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk for
CWD no longer be entered into the animal feed system. Under present
circumstances, FDA is not recommending that feed made from deer and elk from a
non-endemic area be recalled if a State later declares the area endemic for CWD
or a CWD eradication zone. In addition, at this time, FDA is not recommending
that feed made from deer and elk believed to be from a captive herd that
contained no CWD-positive animals be recalled if that herd is subsequently found
to contain a CWD-positive animal. V. Use in animal feed of material from deer
and elk NOT considered at high risk for CWD
FDA continues to consider materials from deer and elk NOT considered at
high risk for CWD to be acceptable for use in NON-RUMINANT animal feeds in
accordance with current agency regulations, 21 CFR 589.2000. Deer and elk not
considered at high risk include: (1) deer and elk from areas not declared by
State officials to be endemic for CWD and/or to be CWD eradication zones; and
(2) deer and elk that were not at some time during the 60-month period
immediately before the time of slaughter in a captive herd that contained a
CWD-positive animal.
that voluntary mad cow feed ban that became law, how did that work out for
us $
***e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
***
ENFORCEMENT REPORT FOR AUGUST 2, 2006
please note, considering .005 grams is lethal, I do not know how much of
this 125 TONS of banned mad cow protein was part of the ;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
bbbut, this was about 10 years post mad cow feed ban from 1997. 10 years
later, and still feeding banned mad cow protein to cervids???
considering that .005 gram is lethal to several bovines, and we know that
the oral consumption of CWD tainted products is very efficient mode of
transmission of CWD.
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall #
V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
***e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
***
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50
lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%,
Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to
20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall #
V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall #
V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email
and visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. *** This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada. *** It also
suggests a similar cause or source for atypical BSE in these countries. ***
see page 176 of 201 pages...tss
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not bear
cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
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
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
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From
Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 -0500
EMC 1 Terry S. Singeltary Sr. Vol #: 1 http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm
PLEASE SEE FULL TEXT SUBMISSION ; http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html
> First transmission of CWD to transgenic mice over-expressing bovine
prion protein gene (TgSB3985)
PRION 2014 - PRIONS: EPIGENETICS and NEURODEGENERATIVE DISEASES – Shaping
up the future of prion research
Animal TSE Workshop 10.40 – 11.05 Talk Dr. L. Cervenakova First
transmission of CWD to transgenic mice over-expressing bovine prion protein gene
(TgSB3985)
P.126: Successful transmission of chronic wasting disease (CWD) into mice
over-expressing bovine prion protein (TgSB3985)
Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana
Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1
1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of
California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA
Keywords: chronic wasting disease, transmission, transgenic mouse, bovine
prion protein
Background. CWD is a disease affecting wild and farmraised cervids in North
America. Epidemiological studies provide no evidence of CWD transmission to
humans. Multiple attempts have failed to infect transgenic mice expressing human
PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal
human PrPC in vitro provides additional evidence that transmission of CWD to
humans cannot be easily achieved. However, a concern about the risk of CWD
transmission to humans still exists. This study aimed to establish and
characterize an experimental model of CWD in TgSB3985 mice with the following
attempt of transmission to TgHu mice.
Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were
intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse
(CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly
injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD)
or elk (CWD/Elk). Animals were observed for clinical signs of neurological
disease and were euthanized when moribund. Brains and spleens were removed from
all mice for PrPCWD detection by Western blotting (WB). A histological analysis
of brains from selected animals was performed: brains were scored for the
severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain
regions.
Results. Clinical presentation was consistent with TSE. More than 90% of
TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres
in the brain but only mice in the latter group carried PrPCWD in their spleens.
We found evidence for co-existence or divergence of two CWD/ Tga20 strains based
on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk
or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen
by WB. However, on neuropathological examination we found presence of amyloid
plaques that stained positive for PrPCWD in three CWD/WTD- and two
CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and
CWD/Elkinfected mice were similar but unique as compared to profiles of BSE,
BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM
mice tested positive for PrPCWD by WB or by immunohistochemical detection.
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
Thursday, November 21, 2013
*** Assessing the susceptibility of transgenic mice over-expressing deer
prion protein to bovine spongiform encephalopathy
The present study was designed to assess the susceptibility of the
prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy
(BSE) prions, which have the ability to overcome species barriers.
Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a
90-100% attack rates, BSE from cattle failed to transmit, indicating agent
adaptation in the deer.
TSS
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
" although the infection rate was low (4 of 13 animals [Hamir et al.
2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly
as possible all updates/comments that contribute substantially to the topic
under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author
Affiliations
1Institute for Neurodegenerative Diseases, University of California, San
Francisco, San Francisco, California 94143 2Department of Neurology, University
of California, San Francisco, San Francisco, California 94143 Correspondence:
stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As
the only prion disease identified in free-ranging animals, CWD appears to be far
more communicable than other forms of prion disease. CWD was first described in
1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of
histopathology of the brain. Originally detected in the American West, CWD has
spread across much of North America and has been reported also in South Korea.
In captive populations, up to 90% of mule deer have been reported to be positive
for prions (Williams and Young 1980). The incidence of CWD in cervids living in
the wild has been estimated to be as high as 15% (Miller et al. 2000). The
development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible
to CWD, has enhanced detection of CWD and the estimation of prion titers
(Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces,
even in presymptomatic deer, has been identified as a likely source of infection
for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD
has been transmitted to cattle after intracerebral inoculation, although the
infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding
raised concerns that CWD prions might be transmitted to cattle grazing in
contaminated pastures.
snip...
----- Original Message -----
From: David Colby To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor
Department of Chemical Engineering University of Delaware
===========END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION
CONGRESS SEPTEMBER 8-11 2010
Sunday, August 19, 2012
Susceptibility of cattle to the agent of chronic wasting disease from elk
after intracranial inoculation 2012
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
these cattle ranchers supporting these shooting pens, if there are any,
could be in terrible shape if a strain of cwd was to jump to cattle...just
saying.
Title: Transmission of chronic wasting disease of mule deer to Suffolk
sheep following intracerebral inoculation
Authors
item Hamir, Amirali item Kunkle, Robert item Cutlip, Randall - ARS RETIRED
item Miller, Janice - ARS RETIRED item Williams, Elizabeth - UNIV OF WYOMING,
LARAMIE item Richt, Juergen
Submitted to: Journal of Veterinary Diagnostic Investigation Publication
Type: Peer Reviewed Journal Publication Acceptance Date: June 20, 2006
Publication Date: November 1, 2006 Citation: Hamir, A.N., Kunkle, R.A., Cutlip,
R.C., Miller, J.M., Williams, E.S., Richt, J.A. 2006. Transmission of chronic
wasting disease of mule deer to Suffolk sheep following intracerebral
inoculation. Journal of Veterinary Diagnostic Investigation. 18(6):558-565.
Interpretive Summary: Chronic wasting disease (CWD) has been identified in
captive and free ranging deer and elk since 1967. To determine the
transmissibility of CWD to sheep and to provide information about the disease
and tests for detection of CWD in sheep, 8 lambs were inoculated with brain
suspension from mule deer naturally affected with CWD. Two other lambs were kept
as controls. Only 1 sheep developed clinical disease at 35 months after
inoculation. The study was terminated at 72 months after the inoculation. At
that time one other sheep was found to be positive for the disease. It is
proposed that the host's genetic makeup may play a role in transmission of the
disease to domestic sheep. Impact. This is the first study which shows that it
is possible to transmit CWD to a small number of sheep. Technical Abstract:
Chronic wasting disease (CWD) has been identified in captive and free-ranging
cervids since 1967. To determine the transmissibility of CWD to sheep and to
provide information about clinical course, lesions, and suitability of currently
used diagnostic procedures for detection of CWD in sheep, 8 Suffolk lambs (4 QQ
and 4 QR at codon 171 of prion protein (PRNP) gene) were inoculated
intracerebrally with brain suspension from mule deer naturally affected with CWD
(CWD**md). Two other lambs (1 QQ and 1 QR at codon 171 of PRNP gene) were kept
as non-inoculated controls. Within 36 months post inoculation (MPI), 2 animals
became recumbent and were euthanized. However, only 1 sheep (euthanized at 35
MPI) had shown clinical signs that were consistent with those of scrapie.
Microscopic lesions of spongiform encephalopathy (SE) were seen in this sheep
and its tissues were positive for the abnormal prion protein (PrPres) by
immunohistochemistry and Western blot. Retrospective examination of the PRNP
genotype of this animal revealed that it was heterozygous (AV) at codon 136. In
the next 24 months, 3 other sheep were euthanized because of conditions
unrelated to TSE. The remaining 3 sheep remained non-clinical at the termination
of the study (72 MPI) and were euthanized at that time. One of these 3 revealed
SE and its tissues were positive for PrPres. These findings demonstrate that it
is possible to transmit CWD**md agent to sheep via the intracerebral route.
However, the host genotype may play a significant part in successful
transmission and incubation period of this agent.
Thus far, among domestic animals, CWDmd has been transmitted by the
intracerebral route to a goat18 and cattle.5–7 The present findings demonstrate
that it is also possible to transmit CWDmd agent to sheep via the intracerebral
route. However, the only sheep to develop clinical TSE within 35 MPI was
genotypically AV at PRNP codon 136, suggesting that host genotype may play a
notable part in successful transmission of the disease in this species. Although
in Suffolk sheep the AV variant at codon 136 is very rare,17 selective breeding
of Suffolk sheep with this codon has begun in the hope of testing this
differential susceptibility hypothesis in a future study of CWDmd transmission
to sheep.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
***please read this***
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
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc
MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C.
Maddison, BSc, PhD3 + Author Affiliations
1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey
KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of
Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS
UK, School of Veterinary Medicine and Science, The University of Nottingham,
Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for
correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and
chronic wasting disease of deer/elk are contagious prion diseases where
environmental reservoirs are directly implicated in the transmission of disease.
In this study, the effectiveness of recommended scrapie farm decontamination
regimens was evaluated by a sheep bioassay using buildings naturally
contaminated with scrapie. Pens within a farm building were treated with either
20,000 parts per million free chorine solution for one hour or were treated with
the same but were followed by painting and full re-galvanisation or replacement
of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype
VRQ/VRQ were reared within these pens and their scrapie status was monitored by
recto-anal mucosa-associated lymphoid tissue. All animals became infected over
an 18-month period, even in the pen that had been subject to the most stringent
decontamination process. These data suggest that recommended current guidelines
for the decontamination of farm buildings following outbreaks of scrapie do
little to reduce the titre of infectious scrapie material and that environmental
recontamination could also be an issue associated with these premises.
SNIP...
Discussion
Thorough pressure washing of a pen had no effect on the amount of
bioavailable scrapie infectivity (pen B). The routine removal of prions from
surfaces within a laboratory setting is treatment for a minimum of one hour with
20,000 ppm free chlorine, a method originally based on the use of brain
macerates from infected rodents to evaluate the effectiveness of decontamination
(Kimberlin and others 1983). Further studies have also investigated the
effectiveness of hypochlorite disinfection of metal surfaces to simulate the
decontamination of surgical devices within a hospital setting. Such treatments
with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower
than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous
treatment of the pen surfaces did not effectively remove the levels of scrapie
infectivity over that of the control pens, indicating that this method of
decontamination is not effective within a farm setting. This may be due to the
high level of biological matrix that is present upon surfaces within the farm
environment, which may reduce the amount of free chlorine available to
inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had
also became scrapie positive within nine months, with all animals in this pen
being RAMALT positive by 18 months of age. Pen D was no further away from the
control pen (pen A) than any of the other pens within this barn. Localised hot
spots of infectivity may be present within scrapie-contaminated environments,
but it is unlikely that pen D area had an amount of scrapie contamination that
was significantly different than the other areas within this building.
Similarly, there were no differences in how the biosecurity of pen D was
maintained, or how this pen was ventilated compared with the other pens. This
observation, perhaps, indicates the slower kinetics of disease uptake within
this pen and is consistent with a more thorough prion removal and
recontamination. These observations may also account for the presence of
inadvertent scrapie cases within other studies, where despite stringent
biosecurity, control animals have become scrapie positive during challenge
studies using barns that also housed scrapie-affected animals (Ryder and others
2009). The bioassay data indicate that the exposure of the sheep to a farm
environment after decontamination efforts thought to be effective in removing
scrapie is sufficient for the animals to become infected with scrapie. The main
exposure routes within this scenario are likely to be via the oral route, during
feeding and drinking, and respiratory and conjunctival routes. It has been
demonstrated that scrapie infectivity can be efficiently transmitted via the
nasal route in sheep (Hamir and others 2008), as is the case for CWD in both
murine models and in white-tailed deer (Denkers and others 2010, 2013).
Recently, it has also been demonstrated that CWD prions presented as dust when
bound to the soil mineral montmorillonite can be infectious via the nasal route
(Nichols and others 2013). When considering pens C and D, the actual source of
the infectious agent in the pens is not known, it is possible that biologically
relevant levels of prion survive on surfaces during the decontamination regimen
(pen C). With the use of galvanising and painting (pen D) covering and sealing
the surface of the pen, it is possible that scrapie material recontaminated the
pens by the movement of infectious prions contained within dusts originating
from other parts of the barn that were not decontaminated or from other areas of
the farm.
Given that scrapie prions are widespread on the surfaces of affected farms
(Maddison and others 2010a), irrespective of the source of the infectious prions
in the pens, this study clearly highlights the difficulties that are faced with
the effective removal of environmentally associated scrapie infectivity. This is
likely to be paralleled in CWD which shows strong similarities to scrapie in
terms of both the dissemination of prions into the environment and the facile
mode of disease transmission. These data further contribute to the understanding
that prion diseases can be highly transmissible between susceptible individuals
not just by direct contact but through highly stable environmental reservoirs
that are refractory to decontamination.
The presence of these environmentally associated prions in farm buildings
make the control of these diseases a considerable challenge, especially in
animal species such as goats where there is lack of genetic resistance to
scrapie and, therefore, no scope to re-stock farms with animals that are
resistant to scrapie.
Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE)
Accepted October 12, 2014. Published Online First 31 October 2014
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
PPo3-22:
Detection of Environmentally Associated PrPSc on a Farm with Endemic
Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh
Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of
Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories
Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University
of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes of
transmission and specifically the role of fomites in transmission remain poorly
defined. Here we present biochemical data demonstrating that on a
scrapie-affected sheep farm, scrapie prion contamination is widespread. It was
anticipated at the outset that if prions contaminate the environment that they
would be there at extremely low levels, as such the most sensitive method
available for the detection of PrPSc, serial Protein Misfolding Cyclic
Amplification (sPMCA), was used in this study. We investigated the distribution
of environmental scrapie prions by applying ovine sPMCA to samples taken from a
range of surfaces that were accessible to animals and could be collected by use
of a wetted foam swab. Prion was amplified by sPMCA from a number of these
environmental swab samples including those taken from metal, plastic and wooden
surfaces, both in the indoor and outdoor environment. At the time of sampling
there had been no sheep contact with these areas for at least 20 days prior to
sampling indicating that prions persist for at least this duration in the
environment. These data implicate inanimate objects as environmental reservoirs
of prion infectivity which are likely to contribute to disease transmission.
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
Sunday, December 21, 2014
Mucosal immunization with an attenuated Salmonella vaccine partially
protects white-tailed deer from chronic wasting disease
Friday, December 19, 2014
Pan-Provincial Vaccine Enterprise Inc. (PREVENT) Conducting a Chronic
Wasting Disease (CWD) Vaccine Efficacy Trial in Elk
CHRONIC WASTING DISEASE CWD TSE PRION, how much does it pay to find CWD
$$$
CWD, spreading it around...
for the game farm industry, and their constituents, to continue to believe
that they are _NOT_, and or insinuate that they have _NEVER_ been part of the
problem, will only continue to help spread cwd. the game farming industry, from
the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet
mills, shooting pens, to large ranches, are not the only problem, but it is
painfully obvious that they have been part of the problem for decades and
decades, just spreading it around, as with transportation and or exportation and
or importation of cervids from game farming industry, and have been proven to
spread cwd. no one need to look any further than South Korea blunder ;
===========================================
spreading cwd around...
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of
farmed elk in Saskatchewan in a single epidemic. All of these herds were
depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease
eradication program. Animals, primarily over 12 mo of age, were tested for the
presence CWD prions following euthanasia. Twenty-one of the herds were linked
through movements of live animals with latent CWD from a single infected source
herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily
infected herds.
***The source herd is believed to have become infected via importation of
animals from a game farm in South Dakota where CWD was subsequently diagnosed
(7,4). A wide range in herd prevalence of CWD at the time of herd depopulation
of these herds was observed. Within-herd transmission was observed on some
farms, while the disease remained confined to the introduced animals on other
farms.
spreading cwd around...
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim,
Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research
Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion
disease in native North America deer and Rocky mountain elks. The disease is a
unique member of the transmissible spongiform encephalopathies (TSEs), which
naturally affects only a few species. CWD had been limited to USA and Canada
until 2000.
On 28 December 2000, information from the Canadian government showed that a
total of 95 elk had been exported from farms with CWD to Korea. These consisted
of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72
elk in 1997, which had been held in pre export quarantine at the “source
farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD
surveillance program was initiated by the Ministry of Agriculture and Forestry
(MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994
were impossible to identify. CWD control measures included stamping out of all
animals in the affected farm, and thorough cleaning and disinfection of the
premises. In addition, nationwide clinical surveillance of Korean native
cervids, and improved measures to ensure reporting of CWD suspect cases were
implemented.
Total of 9 elks were found to be affected. CWD was designated as a
notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and
2005.
Since February of 2005, when slaughtered elks were found to be positive,
all slaughtered cervid for human consumption at abattoirs were designated as
target of the CWD surveillance program. Currently, CWD laboratory testing is
only conducted by National Reference Laboratory on CWD, which is the Foreign
Animal Disease Division (FADD) of National Veterinary Research and Quarantine
Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the
human consumption was confirmed as positive. Consequently, all cervid – 54 elks,
41 Sika deer and 5 Albino deer – were culled and one elk was found to be
positive. Epidemiological investigations were conducted by Veterinary
Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary
services.
Epidemiologically related farms were found as 3 farms and all cervid at
these farms were culled and subjected to CWD diagnosis. Three elks and 5
crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and
confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were
linked to the importation of elks from Canada in 1994 based on circumstantial
evidences.
In December 2010, one elk was confirmed as positive at Farm 5.
Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer –
were culled and one Manchurian Sika deer and seven Sika deer were found to be
positive. This is the first report of CWD in these sub-species of deer.
Epidemiological investigations found that the owner of the Farm 2 in CWD
outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced
from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed
(species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as
negative.
Thursday, July 03, 2014
How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
CWD, spreading it around...
Tuesday, January 06, 2015
APHIS Provides Additional Information on Chronic Wasting Disease (CWD)
Indemnity Requests January 5, 2015 05:26 PM EST
CWD TO HUMANS, AND RISK FACTORS THERE FROM (see latest science)
Tuesday, November 04, 2014
*** Six-year follow-up of a point-source exposure to CWD contaminated
venison in an Upstate New York community: risk behaviours and health outcomes
2005–2011
Saturday, January 31, 2015
RAPID ADVICE 17-2014 : Evaluation of the risk for public health of casings
in countries with a “negligible risk status for BSE” and on the risk of
modification of the list of specified risk materials (SRM) with regard to BSE
Friday, January 23, 2015
*** Replacement of soybean meal in compound feed by European protein
sources and relaxing the mad cow ban $
Saturday, January 24, 2015
Bovine Spongiform Encephalopathy: Atypical Pros and Cons
Comment from Terry Singeltary Sr. This is a Comment on the Animal and
Plant Health Inspection Service (APHIS) Notice: Agency Information Collection
Activities; Proposals, Submissions, and Approvals: Bovine Spongiform
Encephalopathy; Importation of Animals and Animal Products
For related information, Open Docket Folder
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Comment View document:Docket No. APHIS-2014-0107 Bovine Spongiform
Encephalopathy; Importation of Animals and Animal Products Singeltary Submission
;
I believe that there is more risk to the world from Transmissible
Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from
the United States and all of North America, than there is risk coming to the USA
and North America, from other Countries. I am NOT saying I dont think there is
any risk for the BSE type TSE prion coming from other Countries, I am just
saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present
mad cow risk factors in North America like they are not here?
North America has more strains of TSE prion disease, in more species
(excluding zoo animals in the early BSE days, and excluding the Feline TSE and
or Canine TSE, because they dont look, and yes, there has been documented
evidence and scientific studies, and DEFRA Hound study, that shows the canine
spongiform encephalopathy is very possible, if it has not already happened, just
not documented), then any other Country in the world. Mink TME, Deer Elk cervid
CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type
BSE cattle, atyical HG type BSE cow (the only cow documented in the world to
date with this strain), typical sheep goat Scrapie (multiple strains), and the
atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical
Scrapie has spread from coast to coast. sporadic CJD on the rise, with different
strains mounting, victims becoming younger, with the latest nvCJD human mad cow
case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL
CDC.
typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al),
and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical
Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid
populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk
assessments for each country, and then made BSE confirmed countries legal to
trade mad cow disease, which was all brought forth AFTER that fateful day
December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats
the day it all started. once the BSE MRR policy was shoved down every countries
throat by USDA inc and the OIE, then the legal trading of Scrapie was validated
to be a legal trading commodity, also shoved through by the USDA inc and the
OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion
disease typical and atypical strains, and the BSE TSE Prion aka mad cow type
disease was thus made a legal trading commodity, like it or not. its all about
money now folks, trade, to hell with human health with a slow incubating
disease, that is 100% fatal once clinical, and forget the fact of exposure,
sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion
disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its
all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the
infamous VPSPr. ...problem solved $$$
the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was
nothing but ink on paper.
for this very reason I believe the BSE MRR policy is a total failure, and
that this policy should be immediately withdrawn, and set back in place the BSE
GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all
TSE PRION disease in all species of animals, and that the BSE GBR risk
assessments be made stronger than before.
lets start with the recent notice that beef from Ireland will be coming to
America.
Ireland confirmed around 1655 cases of mad cow disease. with the highest
year confirming about 333 cases in 2002, with numbers of BSE confirmed cases
dropping from that point on, to a documentation of 1 confirmed case in 2013, to
date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad
cow feed ban, and the enforcement of that ban, has drastically reduced the
number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the
USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in
2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD
COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in
my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow
disease in the USA, we still have no clue as to the true number of cases of BSE
mad cow disease in the USA or North America as a whole. ...just saying.
Number of reported cases of bovine spongiform encephalopathy (BSE) in
farmed cattle worldwide* (excluding the United Kingdom)
Country/Year
snip...please see attached pdf file, with references of breaches in the
USA triple BSE mad cow firewalls, and recent science on the TSE prion disease.
...TSS No documents available. AttachmentsView All (1) Empty Docket No.
APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and
Animal Products Singeltary Submission View Attachment:
Sunday, January 11, 2015
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission
*** HUMAN MAD COW DISEASE nvCJD TEXAS CASE NOT LINKED TO EUROPEAN TRAVEL
CDC ***
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
in June 2014 confirmed as USA case NOT European ***
the patient had resided in Kuwait, Russia and Lebanon. The completed
investigation did not support the patient's having had extended travel to
European countries, including the United Kingdom, or travel to Saudi Arabia. The
specific overseas country where this patient’s infection occurred is less clear
largely because the investigation did not definitely link him to a country where
other known vCJD cases likely had been infected.
Sunday, December 14, 2014
*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report ***
Thursday, January 15, 2015
41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE
Prion: Case Report
Subject: *** Becky Lockhart 46, Utah’s first female House speaker, dies
diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type
disease
what is CJD ? just ask USDA inc., and the OIE, they are still feeding the
public and the media industry fed junk science that is 30 years old.
why doesn’t some of you try reading the facts, instead of rubber stamping
everything the USDA inc says.
sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and
there is much concern now for CWD and risk factor for humans.
My sincere condolences to the family and friends of the House Speaker Becky
Lockhart. I am deeply saddened hear this.
with that said, with great respect, I must ask each and every one of you
Politicians that are so deeply saddened to hear of this needless death of the
Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am
seriously going to ask you all this...I have been diplomatic for about 17 years
and it has got no where. people are still dying. so, are you all stupid or
what??? how many more need to die ??? how much is global trade of beef and other
meat products that are not tested for the TSE prion disease, how much and how
many bodies is this market worth?
Saturday, January 17, 2015
*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed
with the extremely rare Creutzfeldt-Jakob disease
Thursday, January 22, 2015
Transmission properties of atypical Creutzfeldt-Jakob disease: a clue to
disease etiology?
Tuesday, December 30, 2014
TSEAC USA Reason For Recalls Blood products, collected from a donors
considered to be at increased risk for Creutzfeldt-Jakob Disease (CJD), were
distributed END OF YEAR REPORT 2014
who’s kidding whom $$$ i.e. USDA INC AND THE OIE
2014
***Moreover, L-BSE has been transmitted more easily to transgenic mice
overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
***It has been suggested that some sporadic CJD subtypes in humans may
result from an exposure to the L-BSE agent.
*** Lending support to this hypothesis, pathological and biochemical
similarities have been observed between L-BSE and an sCJD subtype (MV genotype
at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and
another sCJD subtype (MM genotype) [15].
snip...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far
*** but the possibility that a small proportion of human cases so far
classified as "sporadic" CJD are of zoonotic origin could not be excluded.
*** Moreover, transmission experiments to non-human primates suggest that
some TSE agents in addition to Classical BSE prions in cattle (namely L-type
Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME)
and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
*** Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
*** These atypical BSE cases constitute an unforeseen first threat that
could sharply modify the European approach to prion diseases.
Second threat
snip...
Saturday, December 13, 2014
Terry S. Singeltary Sr. Publications TSE prion disease
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
snip...
TSS
