Friday, September 05, 2014

CFIA CWD and Grain Screenings due to potential risk factor of spreading via contamination of grain, oil seeds, etc.

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

0 Comments:

Post a Comment

Subscribe to Post Comments [Atom]

<< Home