CFIA CWD and Grain Screenings due to potential risk factor of spreading via
contamination of grain, oil seeds, etc.
CWD and Grain Screenings
During the recent months the feed industry and cervid producers have been
meeting with the Canadian Food Inspection Agency (CFIA) to deal with potential
spread of Chronic Wasting Disease (CWD) through grain screenings. CWD is a
transmissible spongiform encephalopathy (TSE) of the deer family related to BSE
in cattle. As far as it is known CWD cannot be spread to people or cattle, but
there is still a caution about it.
CWD has been found in Saskatchewan and the eastern part of Alberta. A claim
has been made by CFIA that wild deer and elk carriers could potentially
contaminate grain, oil seeds and swaths through urine, saliva or excreta. Part
of the theory was that CWD prions would end up in the grain and be taken through
to screenings when grain and canola were cleaned. This would be a potential
vector for prion transmission but there has been no scientific verification of
the transmission process. The CFIA has indicated, to date, there are no
commercially available analytical methods available in Canada or other countries
that can detect CWD prions in cereal grain screenings.
Regardless, the CFIA decided to prohibit movement of screenings in the CWD
infected zone in one third of eastern Alberta and Saskatchewan. No screenings
were to be transported out of the region to feedmills or feedlots using those
products. As well, any grain from the zone being cleaned outside the zone, for
example in Vancouver, would require the screenings to be sent back to the CWD
zone. This could disrupt grain screening movement to feedmills and feedlots in
Alberta. There has been limited consultation with the grain or cervid sectors
and limited discussion on how to address this issue by CFIA with the
sectors.
The pending date for the regulation was alleged to be next week. This would
affect the beef cattle feeding sector with restricted movement of screenings as
a feedstock. About 1.5 million tonnes of screenings are produced in Alberta and
Saskatchewan every year, about 500,000 tonnes moves into the feeding sector.
Around one million tonnes is presently exported outside the control zone each
year.
ANAC joins with major grain organizations to oppose CFIA’s control zone
approach to chronic wasting disease
In the June newsletter, we reported that CFIA has proposed using a control
zone approach to control the spread of Chronic Wasting Disease (CWD). This would
restrict the movement of cereal grain screenings within and out of the primary
control zones, those being all of Saskatchewan and parts of southern Alberta.
Since CFIA did not consult the feed industry or any of the key grain industry
stakeholders before developing the control zone proposal, a broad range of
negative, and presumably unintended consequences have emerged during subsequent
analysis by industry.
Therefore, over the past several weeks ANAC has teamed up with other
stakeholders including the grain elevator, milling and malting associations to
prepare a joint submission to the Minister of Agriculture to delineate the
negative economic and logistical impacts of CFIA’s proposed control zone
approach.
CFIA as the developer of the proposal has not provided the scientific and
risk-based evidence to support these extraordinary measures to control CWD.
Thus, our letter to the minister emphasized the fact that restrictions on the
movement of grain screenings would be a misdirected attempt to halt the spread
of the disease, given the improbability that screenings are in fact a
significant disease vector associated with CWD.
We also highlighted to the minister that Canada’s reputation as a reliable
supplier of grains and oilseeds will be undermined if CFIA’s proposal is
implemented. Western Canada supplies cereal crops valued at over $7.0 billion
annually to the export market, with the annual value of exports from
Saskatchewan and Alberta exceeding $3.6 billion and $1.4 billion respectively.
Moreover, the proposed restrictions would adversely affect at least 7 categories
of grain businesses at both the international and domestic levels, including
wheat milling, oat milling, malting, ethanol, feed manufacturing, seed cleaning
and grain handling.
CFIA’s control zone proposal is also unanimously opposed by the cervid
farming industry. Farmers are in agreement that the spread of CWD needs to be
controlled, however they support the use of a farmed-based risk management
system, which is more consistent with CFIA’s mandate to deliver outcome-based
solutions. We are hopeful that the joint submission, signed by the major players
in the feed and grain industries, will prompt CIFA to propose an alternative
workable solution to control CWD.
Joint submission sent to Agriculture Minister objecting restrictions on
movement of screenings
Date:
Wednesday, August 6, 2014
• It is important to know whether plants might take up prions through their
roots systems and be a potential means of transmission of prion diseases. In a
study with wheat plants, Alberta researchers found that prions essentially were
not taken up into the plants through the root systems. (Relevant to long-term
outcomes 2 and 3 and initiatives 1, 2, 4, and 5)
Prion Transmission Through Plants:
•McAllister and collaborators with Alberta Agriculture and Rural
Development and the CFIA worked with Master’s student Jay Rasmussen to explore
Chronic Wasting Disease (CWD) prion’s potential for uptake and transmission by
plants.
•Because plants have the ability to take up proteins, it was hypothesized
that plants could also assimilate prion protein through the root system; if this
was the case, then plants could potentially transmit the disease among wild deer
and elk populations.
•Rasmussen’s work suggested that prions were not taken up into the leaves
and stems of wheat, although they did bind to roots.
•Rasmussen’s work provides evidence that uptake of prions into plants from
soil is unlikely, but further research is necessary before the uptake of prions
into plants can be completely eliminated as a vector of the disease.
Background
The enhanced feed ban regulations prohibit the use of SRM in fertilizers or
fertilizer supplements unless in accordance with a permit issued by the CFIA
under the authority of the Health of Animals Regulations. To obtain a permit,
each proposed use is evaluated on a case by case basis. Currently, the CFIA
would not consider issuing a permit for the domestic use of composted SRM for
the following reasons.
1.SRM are certain cattle tissues capable of transmitting BSE. There is no
human health risk assessment to indicate the absence of human health concerns
associated with use of composted SRM domestically. To date, scientific evidence
has not been able to demonstrate that composting destroys prions. Although
domestic use would pose a negligible risk to livestock, there is a potential
risk to humans via direct ingestion of the compost or of compost particles
adhered to skin or plant material (e.g. carrots). Another potential route of
exposure is by ingestion of prions that have been taken up by plants. It has
been proven that bacteria are readily taken up by some plants (e.g. E. coli in
lettuce) thus the uptake of prions by plants cannot be precluded or dismissed at
this time. As a science-based regulator, the CFIA cannot change the policy on
this issue without a risk assessment demonstrating that the use of composted SRM
poses an acceptable risk to humans.
2.Under the new regulations, permits are required for all handlers of SRM
so that the CFIA may maintain control over this material. Composted SRM is still
considered SRM; therefore every recipient of composted SRM would also require a
permit. This level of oversight would likely prove too onerous for most domestic
users.
Can plants serve as a vector for prions causing chronic wasting
disease?
Jay Rasmussen, Brandon H Gilroyed, Tim Reuter, Sandor Dudas, Norman F
Neumann, Aru Balachandran, Nat NV Kav, Catherine Graham, Stefanie Czub, Tim A
McAllister*View affiliations
Submitted 28 Nov 2013
Revised 10 Jan 2014
Accepted 22 Jan 2014
Published Online 7 Feb 2014
Abstract
Prions, the causative agent of chronic wasting disease (CWD) enter the
environment through shedding of bodily fluids and carcass decay, posing a
disease risk as a result of their environmental persistence. Plants have the
ability to take up large organic particles, including whole proteins, and
microbes. This study used wheat (Triticum aestivum L.) to investigate the uptake
of infectious CWD prions into roots and their transport into aerial tissues. The
roots of intact wheat plants were exposed to infectious prions (PrPTSE) for 24 h
in three replicate studies with PrPTSE in protein extracts being detected by
western blot, IDEXX and Bio-Rad diagnostic tests. Recombinant prion protein
(PrPC) bound to roots, but was not detected in the stem or leaves.
Protease-digested CWD prions (PrPTSE) in elk brain homogenate interacted with
root tissue, but were not detected in the stem. This suggests wheat was unable
to transport sufficient PrPTSE from the roots to the stem to be detectable by
the methods employed. Undigested PrPTSE did not associate with roots. The
present study suggests that if prions are transported from the roots to the
stems it is at levels that are below those that are detectable by western blot,
IDEXX or Bio-Rad diagnostic kits.
SNIP...
In conclusion, our data shows that PrPTSE is not transported to aerial
tissues at concentrations detectable by western blot, however, it still remains
possible for infectious levels to be achieved, especially if significant root
damage occurs. The findings suggest that PK digestion may facilitate the
interaction of PrPTSE with plant roots which is interesting based on the affects
this also has on affinity of these molecules for soil. This study used wheat as
a model but it would be valuable to test native grasses such as crested wheat
grass and fescue which make up a significant portion of the diet of elk and
deer. It is probable that both biotic and abiotic factors affect uptake of
PrPTSE into plants and the introduction of other factors such as soil organisms
and particles into the system is something to consider in future investigations.
Regardless of system, if uptake occurs, animal infectivity assays are needed to
confirm if the prion protein remains in an infective state after plant uptake.
These experiments provide the first known investigation of the involvement of
plants in prion transmission and provide a solid base for future studies.
Friday, September 27, 2013
*** Uptake of Prions into Plants
Presentation Abstract
Title: Uptake of Prions into Plants
Session Title: Current Science of Chronic Wasting Disease: What Have We
Learned in the Last 5 Years?
Session Number: 27
Session Time: Monday, Oct 07, 2013, 8:30 AM -12:20 PM
Presentation Time: Monday, Oct 07, 2013, 11:00 AM -11:20 AM
Presentation Number: 8
Author(s): Christopher Johnson, U.S. Geological Survey, Madison, WI,
Contact: cjjohnson@usgs.gov
Abstract Body:
Chronic wasting disease (CWD) and scrapie-infected animals shed infectious
prions during both the preclinical and clinical phases of disease. Contamination
of environments with prions released from animals or from infected carcasses
appears to contribute to the transmission of these diseases. Previous work has
suggested that soil may serve as an environmental disease reservoir. Vegetation
is ubiquitous in CWD-contaminated environments and plants are known to absorb a
variety of substances from soil, ranging from nutrients to contaminants. The
uptake of proteins from soil into plants has been documented for many years and
we have been investigating the uptake of prions into plants in vitro. Using
laser scanning confocal microscopy, we observed root uptake of
fluorescently-tagged, abnormal prion protein in the model plant Arabidopsis
thaliana, as well as the crop plants alfalfa (Medicago sativa), barley (Hordeum
vulgare) and tomato (Solanum lycopersicum). Using serial protein misfolding
cyclic amplification, a sensitive biochemical prion detection method, we have
found evidence of prions in aerial tissues from these species, as well as maize
(Zea mays). Both stems and leaves of A. thaliana grown in culture media
containing prions are infectious when injected into mice and oral bioassays are
underway for A. thaliana and other plants.
*** Our results suggest that prions are taken up by plants and that
contaminated plants may represent a previously unrecognized risk of human,
domestic species and wildlife exposure to CWD and scrapie agents.
Friday, August 09, 2013
CWD TSE prion, plants, vegetables, and the potential for environmental
contamination
AD.82: Prion-contaminated plants can transmit prion disease
Sandra J. Pritzkow, Rodrigo Morales, Fabio Moda and Claudio Soto
University of Texas Medical School at Houston; Houston. TX USA
Chronic Wasting Disease (CWD) is a prion disorder affecting deer and elk.
The efficient propagation of this disease in captive and free-ranging animals
suggest that it may involve horizontal transmission through contaminated
environment. It has been shown, that infectious prions can enter the environment
through saliva, feces, urine, blood or placenta tissue from infected animals, as
well as by carcasses from diseased animals. Various studies have demonstrated
that infectious prions bind tightly to soil and remain infectious after years in
this material.
We hypothesize that plants, which get in contact with infectious prions,
can also play a role on the horizontal transmission of prion diseases. To study
whether plants can interact with prions, we analyzed wheat grass roots and
leaves incubated with 263K-infected brain homogenate in vitro using the PMCA
technique and in vivo in Syrian hamsters. For in vitro analyses, the plant
tissue was incubated in serial dilutions of 263K-brain homogenate, washed
thoroughly and analyzed for the presence of Prpsc by PMCA. The results show that
even highly diluted Prpsc can bind to roots and leaves and sustain the
conversion of normal prion protein. Similar experiments are currently ongoing
using CWD infected material. In vivo, hamsters were orally infected with leaves
or roots incubated in 10% 263K-infected brain homogenate, which were thoroughly
washed as well.
***Hamsters, inoculated with 263K-contaminated roots or leaves, developed
typical signs of prion disease, whereas control animals inoculated with
non-contaminated plants did not. Prion disease was confirmed by
immunohistological and biochemical analyses.
These findings suggest that plants (leaves and roots) can efficiently bind
infectious prions and act as carrier of infectivity and may play an important
role in horizontal transmission by oral intake of the prion agent.
=====
AD.83: Are plants a potential transmission route for infectious prions?
Jay D. Rasmussen,1,3 Brandon H. Gilroyed,2 Tim Reuter,4 Sandor Dudas,5
Catherine Graham,5 Norman F. Neumann.6 Aru Balachandran,7 Stefanie Czub,5 Nat N.
Kav1 and Tim A. McAllister3
'Department of Agricultural; Food and Nutritional Sciences; University of
Alberta; Edmonton, AB Canada; 2School of Environmental Sciences; University of
Guelph Ridgetown Campus; Ridgetown, ON Canada; 3Agriculture and Aqri-Food
Canada; Lethbridge Research Centre; Lethbridge, AB Canada; 4Alberta Agriculture
and Rural Development; Agriculture Centre; Lethbridge. AB Canada; 5National and
OIE Reference Laboratories of BSE; National Centres for Animal Disease
Lethbridge Laboratory; Canadian Food Inspection Agency; Lethbridge. AB Canada;
School of Public Health; University of Alberta; Edmonton, AB Canada; 'National
and OIE Reference Laboratory for scrapie and CWD; Canadian Food Inspection
Agency; Ottawa ON Canada
Plants are capable of absorbing large organic materials such as proteins
and microorganisms through their roots. This phenomenon introduces the potential
for the uptake of infectious prions from the environment and is a possible route
for the distribution of prion diseases in natural habitats. Wheat (Triticum
aestivum), a major agricultural crop, was used as a model in our experiments to
examine prion uptake by plants. In preliminary experiments, model proteins of
similar size (Q prions were used (fluorescently-tagged ovalbumin, FT-OV;
recombinant cellular PrP, recPrPC). Plants were grown in sterile media
(Murashige and Skoog) for 30-45 d before roots were exposed to a model protein
solution for 24 h. Foreign target proteins were detected by fluorescent
microscopy (FT-OV) and western blotting (FT-OV and recPrPC). FT-OV was found to
enter the root system and translocate to the stem. For recPrPc, no detectable
uptake or translocation was found, but instead, a strong binding of recPrPc to
the outer root surface was observed. These results suggest that uptake by wheat,
although possible, might not be universal for all proteins. The consideration of
how different plants may respond and how natural root damage may affect protein
transport is important. The model described above was used to determine how
infectious prions interact with wheat plants. Wheat roots were exposed for 24 h
to Chronic Wasting Disease positive and negative elk brain homogenates that were
either digested with proteinase K (PK) or left undigested. Plant extracts were
analyzed by western blotting to determine the presence of prion proteins, Bands
corresponding to PK-sensitive prions were detected in root extracts, but not in
other regions of the plant. These results suggest that, similar to model work
with recPrPc, PrPc may bind to the outside of the root, without translocation to
other areas of the plant. Current work is investigating the implications of
exposure of wheat roots to purified PrPCWD on uptake. Future studies will
consider the impact of soil on absorption of PrPCWD by roots. Binding of PrPCWD
to the surface of wheat roots as shown for PrPc, would open a new discussion on
the distribution of infectious prions in the environment.
=====
AD.81: Detection of prion protein associated with cervid chronic wasting
disease in environmental samples
Chad J. Johnson, Christen B. Smith, Michael D. Samuel and Joel A. Pedersen
University of Wisconsin; Madison. WI USA
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy
(TSE) or prion disease affecting North American members of the deer family
(cervids). The disease agent may enter the environment through decomposition of
carcasses and shedding in feces, saliva, and urine. Once in the environment
disease associated prion protein (PrPTSE) can bind to soil components and remain
bioavailable for extended time periods. Assessment of the environmental load of
the disease agent is difficult because relevant levels are below the detection
limits of immunochemical methods and bioassay is prohibitively expensive to use
as a surveillance technique. Here, we report that a combination of detergent
extraction and protein misfolding cyclic amplification with beads (PMCAb)
substantially improves the sensitivity of PrPTSE detection in environmental
samples. Using this technique we are able to achieve detection limits
substantially lower than animal bioassay. Working with amended soils we are able
to extract and amplify PrPTSE to detectable levels. We have investigated factors
contributing to PMCAb inhibition and methods to circumvent those inhibitions.
This technique holds promise for helping to clarify the relative importance of
direct and indirect transmission of CWD, assess the effectiveness of
environmental remediation, and determine environmental loads of infectious
agent.
=====
AD.80: Kinetics of chronic wasting disease prion shedding in cervid saliva
and urine
Nicholas J. Haley, Davin Henderson, Glenn C. Telling and Edward A. Hoover
Colorado State University; Fort Collins. CO USA
Efficient horizontal transmission is a unique hallmark of chronic wasting
disease (CWD) of deer, elk, and moose. Saliva trans- fer, for example via
grazing or mutual grooming, is thought to be the primary mechanism of horizontal
transmission, although urine and feces are also thought ro play an important
role. It is not known how shortly after exposure an animal may begin shedding
PrPCWD, though it has been reported that both clinical and pre-clinical animals
may successfully transmit CWD to naive deer. We hypothesized that transmission
would occur primarily in end-stage disease, though the purpose of this study was
to identify earlier time points during the course of CWD infection in which
saliva and urine may carry infectivity. Using both transgenic mouse bioassay and
real-rime quaking-induced conversion (RT-QuIC), we evaluated saliva and urine
from two experimentally infected white tail deer for which samples were
available from multiple time points post-inoculation (p.i.) (e.g., 3, 6 and 12
mo p.i., as well as immediately prior to euthanasia at 24-27 mos). We found that
while saliva collected during clinical disease was infectious in mouse bioassay,
saliva collected 12 mo p.i., prior to the onset of clinical signs was also
variably infectious. Saliva from time points earlier than 12 mo p.i. failed to
transmit infection, while urine collected from clinically affected deer had very
low potential to transmit infection, as has been reported previously. These
findings extend our understanding of CWD shedding in the natural host, and may
improve control of CWD transmission in captive and free-ranging settings.
www.landesbioscience.com PRION UPDATE VIA VEGETABLE PLANTS FROM THE SOIL
56. Members considered that there is no evidence that crops grown on the
land which received composted excreta from BSE-challenged animals pose a TSE
risk to humans or animals. One member suggested that, as some of these animals
are orally challenged with high doses of BSE-infected materials, and the
distribution of infectivity in the digestive system is not completely
understood, it might be premature to conclude that there is no infective agent
in the manure.
***Furthermore, an unpublished study had indicated low level absorption of
PrP from soil by tomato plants although it should be noted that this study had
not been repeated. Details of this work would be sent to the SEAC Secretary. Dr
Matthews explained that most of the manure from animals challenged with high
doses of BSE had already been composted and used for coppicing. Members agreed
that the risks from disposal of residual manure from experimental animals would
be much less than historic risks of on farm contamination from naturally
infected animals at the height of the BSE epidemic. ...
SNIP...END
SRM are certain cattle tissues capable of transmitting BSE. There is no
human health risk assessment to indicate the absence of human health concerns
associated with use of composted SRM domestically. To date, scientific evidence
has not been able to demonstrate that composting destroys prions. Although
domestic use would pose a negligible risk to livestock, there is a potential
risk to humans via direct ingestion of the compost or of compost particles
adhered to skin or plant material (e.g. carrots). Another potential route of
exposure is by ingestion of prions that have been taken up by plants. It has
been proven that bacteria are readily taken up by some plants (e.g. E. coli in
lettuce) thus the uptake of prions by plants cannot be precluded or dismissed at
this time. As a science-based regulator, the CFIA cannot change the policy on
this issue without a risk assessment demonstrating that the use of composted SRM
poses an acceptable risk to humans.
Saturday, March 10, 2012
CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein
feed CUSTOM MADE for deer and elk
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester
Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE
BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences &
Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s
Hospital London and William Harvey Hospital Ashford April 1999
snip...
88. Natural decay: Infectivity persists for a long time in the environment.
A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep,
after they had grazed on land which had previously been grazed by
scrapie-infected sheep, even though the land had lain fallow for three years
before the healthy sheep were introduced. Brown also quoted an early experiment
of his own (1991), where he had buried scrapie-infected hamster brain and found
that he could still detect substantial infectivity three years later near where
the material had been placed. 89. Potential environmental routes of infection:
Brown discusses the various possible scenarios, including surface or subsurface
deposits of TSE-contaminated material, which would lead to a build-up of
long-lasting infectivity. Birds feeding on animal remains (such as gulls
visiting landfill sites) could disperse infectivity. Other animals could become
vectors if they later grazed on contaminated land. "A further question concerns
the risk of contamination of the surrounding water table or even surface water
channels, by effluents and discarded solid wastes from treatment plants. A
reasonable conclusion is that there is a potential for human infection to result
from environmental contamination by BSE-infected tissue residues. The potential
cannot be quantified because of the huge numbers of uncertainties and
assumptions that attend each stage of the disposal process". These comments,
from a long established authority on TSEs, closely echo my own statements which
were based on a recent examination of all the evidence. 90. Susceptibility: It
is likely that transmissibility of the disease to humans in vivo is probably
low, because sheep that die from scrapie and cattle that die from BSE are
probably a small fraction of the exposed population. However, no definitive data
are available.
91. Recommendations for disposal procedures: Brown recommends that material
which is actually or potentially contaminated by BSE should be: 1) exposed to
caustic soda; 2) thoroughly incinerated under carefully inspected conditions;
and 3) that any residue should be buried in landfill, to a depth which would
minimise any subsequent animal or human exposure, in areas that would not
intersect with any potable water-table source.
92. This review and recommendations from Brown have particular importance.
Brown is one of the world's foremost authorities on TSEs and is a senior
researcher in the US National Institutes of Health (NIH). It is notable that
such a respected authority is forthright in acknowledging the existence of
potential risks, and in identifying the appropriate measures necessary to
safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M
Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will,
"Geographical distribution of variant CJD in the UK (excluding Northern
Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41
(02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD
(variant CJD) might live closer to rendering factories than would be expected by
chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were
studied. The incubation period of vCJD is not known but by analogy with other
human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure
to rendering products, such exposure might plausibly have occurred 8-10 years
before the onset of symptoms. The authors were able to obtain the addresses of
all rendering plants in the UK which were in production in 1988. For each case
of vCJD, the distance from the place of residence on 1st January 1998 to the
nearest rendering plant was calculated
snip...
> After 230 days of composting, only one in five hamsters succumbed to
TSE disease...
composting TSE prions is an accident waiting to happening, absolutely
foolish in my opinion...tss
SRM are certain cattle tissues capable of transmitting BSE. There is no
human health risk assessment to indicate the absence of human health concerns
associated with use of composted SRM domestically. To date, scientific evidence
has not been able to demonstrate that composting destroys prions. Although
domestic use would pose a negligible risk to livestock, there is a potential
risk to humans via direct ingestion of the compost or of compost particles
adhered to skin or plant material (e.g. carrots). Another potential route of
exposure is by ingestion of prions that have been taken up by plants. It has
been proven that bacteria are readily taken up by some plants (e.g. E. coli in
lettuce) thus the uptake of prions by plants cannot be precluded or dismissed at
this time. As a science-based regulator, the CFIA cannot change the policy on
this issue without a risk assessment demonstrating that the use of composted SRM
poses an acceptable risk to humans.
Friday, September 27, 2013
Uptake of Prions into Plants
Presentation Abstract
Friday, August 09, 2013
CWD TSE prion, plants, vegetables, and the potential for environmental
contamination
In conclusion, our results provide compelling support for the hypothesis
that soil serves as a biologically relevant reservoir of TSE infectivity. Our
data are intriguing in light of reports that naïve animals can contract TSEs
following exposure to presumably low doses of agent in the environment [5,7–9].
We find that Mte enhances the likelihood of TSE manifestation in cases that
would otherwise remain subclinical (Figure 3B and 3C), and that prions bound to
soil are orally infectious (Figure 5). Our results demonstrate that adsorption
of TSE agent to inorganic microparticles and certain soils alter transmission
efficiency via the oral route of exposure.
*** 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
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Sunday, August 24, 2014
USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program
Goals TSE PRION October 17 – 23, 2013
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 CHRONIC WASTING DISEASE CWD
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM
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...
>>>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 $
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
###
Rangen, Inc,
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
-------- Original Message --------
Subject: 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
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on; Docket 03D-0186FDA Issues Draft Guidance
on Use of Material From Deer and Elk in Animal Feed; Availability Several
factors on this apparent voluntary proposal disturbs me greatly, please allow me
to point them out;
snip...
Oral transmission and early lymphoid tropism of chronic wasting
diseasePrPres in mule deer fawns (Odocoileus hemionus ) These results indicate
that CWD PrP res can be detected in lymphoid tissues draining the alimentary
tract within a few weeks after oral exposure to infectious prions and may
reflect the initial pathway of CWD infection in deer. The rapid infection of
deer fawns following exposure by the most plausible natural route is consistent
with the efficient horizontal transmission of CWD in nature and enables
accelerated studies of transmission and pathogenesis in the native
species.
snip...
now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr."
Reply-To: BSE-LTo: BSE-L
8420-20.5% Antler DeveloperFor Deer and Game in the wildGuaranteed Analysis
Ingredients / Products Feeding Directions
snip...
_animal protein_
snip...
DEPARTMENT OF HEALTH & HUMAN SERVICESPUBLIC HEALTH SERVICEFOOD AND DRUG
ADMINISTRATIONApril 9, 2001 WARNING LETTER01-PHI-12CERTIFIED MAILRETURN RECEIPT
REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy
Lake, PA 16145
PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:Food and Drug Administration Investigator Gregory E.
Beichner conducted an inspection of your animal feed manufacturing operation,
located in Sandy Lake, Pennsylvania, on March 23,2001, and determined that your
firm manufactures animal feeds including feeds containing prohibited materials.
The inspection found significant deviations from the requirements set forth in
Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins
Prohibited in Ruminant Feed. The regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such
deviations cause products being manufactured at this facility to be misbranded
within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic
Act (the Act).Our investigation found failure to label your swine feed with the
required cautionary statement "Do Not Feed to cattleor other Ruminants" The FDA
suggests that the statement be distinguished by different type-size or color or
other means of highlighting the statement so that it is easily noticed by a
purchaser.
In addition, we note that you are using approximately 140 pounds of cracked
corn to flush your mixer used in the manufacture of animal feeds containing
prohibited material. This flushed material is fed to wild game including deer, a
ruminant animal.Feed material which may potentially contain prohibited material
should not be fed to ruminant animals which may become part of the food
chain.The above is not intended to be an all-inclusive list of deviations
fromthe regulations. As a manufacturer of materials intended for animalfeed use,
you are responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance withthe law. We have enclosed a
copy of FDA's Small Entity Compliance Guideto assist you with complying with the
regulation...
snip...end...full text ;
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In
Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #: 1
see my full text submission here ;
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
TSS
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