Tuesday, June 11, 2013

Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant deviations from requirements in FDA regulations that are intended to reduce the risk of bovine spongiform encephalopathy (BSE) within the United States

Subject: Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant deviations from requirements in FDA regulations that are intended to reduce the risk of bovine spongiform encephalopathy (BSE) within the United States.


Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12


Department of Health and Human Services Public Health Service Food and Drug Administration Denver District Office Bldg. 20-Denver Federal Center P.O. Box 25087 6th Avenue & Kipling Street Denver, Colorado 80225-0087 Telephone: 303-236-3000 FAX: 303-236-3100


June 1, 2012


WARNING LETTER


VIA UPS


Mr. Stephen K. Ulrich Ms. Lonna A. Ulrich Co-Owners Weld County Bi-Products, Inc. 1138 N. 11th Ave. Greeley, CO 80631


Ref. #: DEN-12-16-WL


Dear Mr. and Ms. Ulrich:


Investigators from the U.S. Food and Drug Administration (FDA) conducted inspections of your rendering facility located at 1138 North 11th Avenue, Greeley, Colorado (Greeley Facility) from April 29 to May 9, 2011, and from November 1 to 3, 2011. FDA also conducted inspections of your rendering facility doing business as Fort Morgan Pet Foods, located at 13553 County Road 19, Fort Morgan, Colorado (Fort Morgan Facility) from June 14 to 17, 2011, and from December 5 to 7, 2011.


These inspections revealed significant deviations from requirements in FDA regulations that are intended to reduce the risk of bovine spongiform encephalopathy (BSE) within the United States. These regulations are found in Title 21 of the Code of Federal Regulations (CFR), section 589.2000 (Animal proteins prohibited in ruminant feed) and section 589.2001 (Cattle materials prohibited in animal food or feed to prevent the transmission of bovine spongiform encephalopathy). These regulations address how renderers process (1) mammalian proteins prohibited from use in ruminant food or feed, and (2) materials designated as “cattle materials prohibited in animal food or feed” (CMPAF) which are prohibited from use in animal food or feed. CMPAF include, but are not limited to:


The brain and spinal cord of cattle 30 months of age or older


The entire carcass of cattle infected with BSE


The entire carcass of cattle 30 months or older that have not been inspected and passed for human consumption if the brains and spinal cords were not effectively removed or otherwise effectively excluded from animal feed


Your facilities process CMPAF.


Your failure to follow certain requirements of these regulations as described below resulted in products manufactured and distributed by your facilities being adulterated within the meaning of Section 402(a)(4) of the Federal Food, Drug, and Cosmetic Act (the Act), [21 U.S.C. § 342(a)(4)] and misbranded within the meaning of Section 403(f) of the Act, [21 U.S.C. § 343(f)]. You can find the Act and its associated regulations on the Internet through links on the FDA’s web page at www.fda.gov1.


Adequate Written Procedures


Because your facilities (1) remove the brain and spinal cord from cattle not inspected and passed for human consumption and (2) separate cattle not inspected and passed for human consumption that are 30 months of age or older as a means of ensuring that CMPAF are not introduced into animal food or feed, you must maintain adequate written procedures specifying how these processes are carried out, 21 CFR § 589.2001(c)(2)(ii). Your written procedures are not adequate. Specifically, the hand-written document you supplied to us explaining your procedures for the removal and handling of CMPAF at the Greeley Facility was illegible, and did not completely describe the process of removing, segregating, documenting and disposing of CMPAF at the firm. This document did not explain who would do the work, how it would be done, how the CMPAF would be segregated, what equipment would be used, and how the equipment would be cleaned. At the Fort Morgan Facility, the document titled “Our plan of action to determine age of carcass and dispose of all carcasses 30 months of age and older” explains that your employees have been trained how to age cattle, and that cattle found to be 30 months of age or older are tagged with a (b)(4), but it also lacks information on how removal of the CMPAF would be done, how the material will be segregated, what equipment would be used, and how the equipment would be cleaned.


Record-Keeping


FDA regulations require that you establish, maintain, and make available to FDA for inspection and copying records sufficient to track CMPAF to ensure such material is not introduced into animal feed, 21 CFR § 589.2001(c)(2)(vi). At the Greeley Facility, the only documentation you provided to FDA was a hand-written notebook documenting the date and number of cattle over 30 months of age received at your firm. You did not have documentation to demonstrate that CMPAF is disposed of in a manner to prevent it from entering animal feed. At your Fort Morgan facility, you were using a dry-erase board to track cattle and their CMPAF on a daily basis, but there was not a system in place to save this information or allow for the review and copying of records from days prior to the current day to ensure CMPAF was not introduced into animal feed. We note that on December 5, 2011, the manager of your Fort Morgan firm did provide FDA with copies of a new document, which she indicated, would be used to ensure CMPAF is not introduced into animal feed. We will evaluate how well the new record works at our next inspection.


Avoiding Cross-Contamination


Once CMPAF has been separated from the cattle materials that may be used in feed, 21 CFR § 589.2001(c)(2)(iii) requires the use of measures to avoid cross-contamination, including using separate containers that adequately prevent contact between CMPAF and animal feed, animal feed ingredients, or equipment surfaces. FDA investigators observed that not all of the containers used to hold CMPAF could be differentiated from containers used to hold material that may be used for feed. This lack of differentiation can create confusion and thus does not adequately prevent CMPAF contact with material that may be used in animal feed. At your Fort Morgan facility, a white container used to store CMPAF was observed without any marking to make clear that it is used for CMPAF. At your Greeley facility, FDA investigators observed that neither the truck used to store CMPAF before delivery to the landfill nor a gray bucket in the head-splitting room used to store removed brains from cattle 30 months of age and older were marked to make clear that they were used to store CMPAF. At the close of the November 3, 2011 inspection at the Greeley facility, you indicated that you had added markings to the gray bucket and truck.


Ruminant Feed Caution Statements


At your Greeley Facility the shrink-wrapped pallets of frozen inedible beef to be shipped for further processing into animal feed were not labeled with the “Do not feed to cattle or other ruminants” caution statement required by 21 CFR § 589.2000(c)(1)(i).


This letter is not intended to serve as an all-inclusive list of violations at your facilities. As a manufacturer of materials intended for use in food for animals, you are responsible for ensuring your overall operation and the products you manufacture and distribute comply with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.


As a final matter, the regulation at 21 CFR § 559.2001(c)(2)(v) states that CMPAF and products that contain or may contain CMPAF must be marked with an agent that can be readily detected on visual inspection. Investigators observed at both facilities that you are currently using charcoal to both mark material that needs to be handled as CMPAF, and to decharacterize the animal tissue being harvested and frozen for distribution to a feed manufacturer for further processing. We would like to clarify the discussion you had with the investigators on this topic, and advise you that you should use a different agent to mark the product that must go to disposal than you use to decharacterize product that will be further processed into animal feed so these products may be easily differentiated and not inadvertently confused or commingled.


You should notify this office in writing of the steps you have taken to bring your firm into compliance with the law within fifteen (15) working days of receiving this letter. Your response should include each step that has been taken or will be taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within fifteen (15) working days, state the reason for the delay and the timeframe within which the corrections will be completed. Please include copies of any available documentation demonstrating that corrections have been made.


Your written response should be sent to: William H. Sherer, Compliance Officer, U.S. Food and Drug Administration, P.O. Box 25087 (6th Ave. and Kipling St., DFC, Bldg 20), Denver, CO 80225-0087. If you have any questions about this letter, please contact Mr. Sherer at (303) 236-3051, or by email at william.sherer@fda.hhs.gov.


Sincerely,


/S/ LaTonya M. Mitchell Denver District Director


cc: Ms. Rebecca A. Jones Manager Weld County Bi-Products 13553 County Road 19 Fort Morgan, CO 80701


Ronald C. Nelson, D.V.M. Denver District Manager USDA/FSIS PO Box 25387 DFC, Bldg 45 Denver, CO 80225 -






I would sure like to see the full reports of just these ;




4018 CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y


9367 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N


9446 DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N


9447 DEN-DO 3002857110 Weld County Bi-Products dba Fort Morgan Pet Foods 13553 County Road 19 Fort Morgan CO 80701-7506 OPR RE HP 12/7/2011 OAI N




Thursday, June 6, 2013


BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI ratings as at June 5, 2013






Friday, March 8, 2013


Dogs may have been used to make Petfood and animal feed






Monday, March 26, 2012


CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE






From: LUISA DE RISIO


Sent: Wednesday, April 25, 2012 3:27 AM


To: Terry S. Singeltary Sr.


Subject: RE: Slowly progressive lymphohistiocytic meningoencephalomyelitis in 21 adult cats presenting with peculiar neurological signs


Thanks Terry, I have forwarded your very interesting email to the neuropathologist who looked at these cats’ brains. I will let you know if he discovers anything interesting or if he wants to get in touch with you.


Best regards,


Luisa


-- Luisa De Risio


DMV, MRCVS, PhD, DECVN, European and RCVS recognised specialist in veterinary neurology


Head of Neurology/ Neurosurgery Unit


Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, CB8 7UU Switchboard: 01638 552700 Reg Charity No 209642




From: Terry S. Singeltary Sr.


Sent: Monday, April 23, 2012 3:18 PM


To: BSE-L BSE-L Cc: CJDVOICE CJDVOICE ; bloodcjd bloodcjd


Subject: Slowly progressive lymphohistiocytic meningoencephalomyelitis in 21 adult cats presenting with peculiar neurological signs


Slowly progressive lymphohistiocytic meningoencephalomyelitis in 21 adult cats presenting with peculiar neurological signs


Luisa De Risio1, Richard Brown2, Bryn Tennant3, Andy Sparkes4, Lara Matiasek1,5, Alberta de Stefani1, Herbert Weissenböck6 and Kaspar Matiasek1,7


Abstract


Twenty-one cats presented with a history of slowly progressive neurological signs characterised by a stiff extended tail, behavioural changes, and spastic and ataxic gait. All cats had outdoor access and lived in the same geographical rural area in north-east Scotland. Histological findings were consistent with lymphohistiocytic meningoencephalomyelitis. Immunohistochemistry ruled out 15 pathogens and showed a significant expression of the interferon-inducible Mx protein, suggesting an as yet unidentified infective or environmental immunogenic trigger as the possible causative agent. The late age at onset (mean 9 years), the very slow progression of clinical signs (mean 11 months) and the peculiar clinical presentation (particularly the posture of the tail) have not been reported previously in cats with lymphohistiocytic meningoencephalomyelitis.




could this be a Transmissible Spongiform Encephalopathy TSE Prion mad cow type disease in cats, aka Feline Spongiform Encephalopathy or typical or atypical form ???


From: Terry S. Singeltary Sr.


Sent: Friday, April 20, 2012 8:11 PM


To: xxxxxx


Subject: Slowly progressive lymphohistiocytic meningoencephalomyelitis in 21 adult cats presenting with peculiar neurological signs


Hello Dr. Luisa De Risio et al,


A kind and warm greetings from Bacliff, Texas.


I read this study with great interest. If you don’t mind, I have several questions please.


How was Feline Spongiform Encephalopathy FSE TSE prion disease ruled out ???


Were any testing done for the FSE TSE prion disease of either the typical or the atypical strains ???


Thank You,


kind regards, terry


==========================================


From: LUISA DE RISIO


Sent: Monday, April 23, 2012 3:39 AM


To: Terry S. Singeltary Sr.


Subject: RE: Slowly progressive lymphohistiocytic meningoencephalomyelitis in 21 adult cats presenting with peculiar neurological signs


Hi Terry,


None of these cats’ brains had any of the histological features of FSE.


regards,


Luisa


--


Luisa De Risio


DMV, MRCVS, PhD, DECVN, European and RCVS recognised specialist in veterinary neurology


Head of Neurology/ Neurosurgery Unit


Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, CB8 7UU Switchboard: 01638 552700 Reg Charity No 209642


=================END...TSS...2012==================


> histological features of FSE




this concerns me.


WHAT about sub-clinical TSE prion disease, with no lesions ?


“Histological and biochemical analysis of the brain from this animal failed to show any lesions typical of TSE or PrPsc”


Rabbits are not resistant to prion infection




SNIP...


Edited by Reed B. Wickner, National Institutes of Health, Bethesda, MD, and approved February 16, 2012 (received for review December 6, 2011)


Abstract


The ability of prions to infect some species and not others is determined by the transmission barrier. This unexplained phenomenon has led to the belief that certain species were not susceptible to transmissible spongiform encephalopathies (TSEs) and therefore represented negligible risk to human health if consumed. Using the protein misfolding cyclic amplification (PMCA) technique, we were able to overcome the species barrier in rabbits, which have been classified as TSE resistant for four decades. Rabbit brain homogenate, either unseeded or seeded in vitro with disease-related prions obtained from different species, was subjected to serial rounds of PMCA. De novo rabbit prions produced in vitro from unseeded material were tested for infectivity in rabbits, with one of three intracerebrally challenged animals succumbing to disease at 766 d and displaying all of the characteristics of a TSE, thereby demonstrating that leporids are not resistant to prion infection. Material from the brain of the clinically affected rabbit containing abnormal prion protein resulted in a 100% attack rate after its inoculation in transgenic mice overexpressing rabbit PrP. Transmissibility to rabbits (>470 d) has been confirmed in 2 of 10 rabbits after intracerebral challenge. Despite rabbits no longer being able to be classified as resistant to TSEs, an outbreak of “mad rabbit disease” is unlikely.




“None of the carcasses revealed gross lesions”




Experimental inoculation of raccoons (Procyon lotor) with Spiroplasma mirum and transmissible mink encephalopathy (TME)


Amir N. Hamir, Justin J. Greenlee, Thad B. Stanton, Jodi D. Smith, Stephanie Doucette, Robert A. Kunkle, Judith A. Stasko, Juergen A. Richt, Marcus E. Kehrli, Jr.


Ab s t r a c t


Article


18 The Canadian Journal of Veterinary Research 2011;75:18–24 Experimental inoculation of raccoons (Procyon lotor) with Spiroplasma mirum and transmissible mink encephalopathy (TME) Amir N. Hamir, Justin J. Greenlee, Thad B. Stanton, Jodi D. Smith, Stephanie Doucette, Robert A. Kunkle, Judith A. Stasko, Juergen A. Richt, Marcus E. Kehrli, Jr.


Ab s t r a c t


The primary objective of this study was to determine whether or not Spiroplasma mirum would be capable of producing lesions of transmissible spongiform encephalopathy (TSE) when inoculated in raccoons (Procyon lotor) and, if that was possible, to compare the clinicopathological findings with those of transmissible mink encephalopathy (TME) in the same experimental model. For this purpose, 5 groups (n 5 5) of raccoon kits were inoculated intracerebrally with either S. mirum and/or TME. Two other groups (n 5 5) of raccoon kits served as sham-inoculated controls. All animals inoculated with TME, either alone or in combination, showed clinical signs of neurologic disorder and were euthanized within 6 mo post-inoculation (MPI). None of the carcasses revealed gross lesions. Spongiform encephalopathy was observed by light microscopy and the presence of abnormal disease-causing prion protein (PrPd) was detected by immunohistochemistry (IHC) and Western blot (WB) techniques in only the raccoons administered TME. ...






Experimental Second Passage of Chronic Wasting Disease (CWDmule deer) Agent to Cattle


Microscopical examination of HE-stained sections of brain and spinal cord (cervical, thoracic and lumbar) failed to reveal lesions of spongiform encephalopathy in any of the experimental animals. A few isolated neurons with single, clear vacuoles of variable size were seen in the red nucleus of four inoculated animals (593, 595, 590 and 589). Also, the central canal in the caudal medulla of animal 593 showed a focal area of protrusion of neuropil with some glial cell infiltrations into the canal (Fig. 1). Neither increased gliosis nor degenerate neurons were seen in central nervous system (CNS) tissues. Significant lesions, apart from a few sarcocysts in striated muscles, were not observed in any of the animals.




b) Diagnostic examination


i) Histological examination


Histopathology is no longer the diagnostic method of choice for investigation of suspect animals, or screening of healthy populations. However, an awareness of the histopathological changes is important, to facilitate detection of cases when conducting routine diagnostic histological examinations of cattle brains. For differential diagnosis, sections of medulla–obex are cut at 5 μm thickness and stained with haematoxylin and eosin (H&E). If tissue quality permits, the histopathological examination of H&E sections allows confirmation of the characteristic neuropathological changes of BSE (30, 36) by which the disease was first detected as a spongiform encephalopathy. These changes comprise mainly spongiform change and neuronal vacuolation and are closely similar to those of all other animal TSEs, but in BSE the high frequency of occurrence of neuroparenchymal vacuolation in certain anatomic nuclei of the medulla oblongata at the level of the obex, provides a satisfactory means of establishing a histopathological diagnosis on a single section of the medulla (34) in clinical suspect cases. As in other species, vacuolar changes in the brains of cattle, particularly vacuoles within neuronal perikarya of the red and oculomotor nuclei of the midbrain are an incidental finding (18). The histopathological diagnosis of BSE must therefore not rely on the presence of vacuolated neurons alone, particularly in these anatomical locations.


The diagnosis may be confirmed if completely typical morphological changes are present in the medulla at the level of the obex, but, irrespective of the histopathological diagnosis, immunohistochemistry is now routinely employed in addition, as unpublished evidence suggests that as many as 5% of clinical suspects (which are negative on H&E section examination for vacuolar changes at the obex) can be diagnosed by IHC examination. Clearly, this protocol, confined to examination of the medulla–obex, does not allow a full neuropathological examination for differential diagnoses to be established, nor does it allow a comprehensive phenotypic characterisation of any TSE. It is for this reason that it is recommended that whole brains are removed from all clinical suspects.


OIE Terrestrial Manual 2008






2012


Confirmation of a clinical diagnosis of BSE in cattle is based on recognition of distinctive histopathological changes in the CNS, with confirmation by immunohistochemistry on the fixed tissues, by immunochemistry (western blot, ELISA) on unfixed CNS tissue, or by detection of SAFs. There are no serological assays for BSE, as no specific immune response is recognised as part of the disease process. Table 1.1 shows the tests for BSE that are currently used for diagnosis in Australia






PET FOODS MAD CATS AND MAD DOGS BSE/TSEs


worse still, there is serious risk the media could get to hear of such a meeting...


snip...


Crushed heads (which inevitably involve brain and spinal cord material) are used to a limited extent but will also form one of the constituent raw materials of meat and bone meal, which is used extensively in pet food manufacturer...






2. The Parliamentary Secretary said that he was concerned about the possibility that countries in which BSE had not yet been detected could be exporting raw meat materials (in particular crushed heads) contaminated with the disease to the UK for use in petfood manufacture...


snip...


YOU explained that imported crushed heads were extensively used in the petfood industry...






In particular I do not believe one can say that the levels of the scrapie agent in pet food are so low that domestic animals are not exposed...








some 100+ _documented_ TSE cats of all types later...tss


on occassions, materials obtained from slaughterhouses will be derived from sheep affected with scrapie or cattle that may be incubating BSE for use in petfood manufacture...






*** Meldrum's notes on pet foods and materials used






*** BSE & Pedigree Petfoods ***






FELINE SPONGIFORM ENCEPHALOPATHY FSE










TSE & HOUNDS


GAH WELLS (very important statement here...TSS)


HOUND STUDY


AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.


snip...






76 pages on hound study;


snip...






The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.


38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.


39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.


40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.


41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.


Histopathological support to various other published MAFF experiments




42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).






It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.




2005


DEFRA Department for Environment, Food & Rural Affairs


Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk


GTN: FAX:


Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518


21 November 2001


Dear Mr Singeltary


TSE IN HOUNDS


Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.


As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.


Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.


Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less




As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.


Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK


You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.


I hope this is helpful


Yours sincerely 4


HUGH MCDONAGH BSE CORRESPONDENCE SECTION




======================================


HOUND SURVEY


I am sorry, but I really could have been a co-signatory of Gerald's minute.


I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding.


If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service.


J W WILESMITH Epidemiology Unit 18 October 1991


Mr. R Bradley


cc: Mr. G A H Wells




3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.




Monday, March 26, 2012


CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE


OR-09 15:10 - 15:25 CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE David












Rangen Inc 2/11/10


Department of Health and Human Services Public Health Service Food and Drug Administration


Seattle District Pacific Region 22201 23rd Drive SE Bothell, WA 98021-4421 Telephone: 425-486-8788 FAX: 425-483-4996


February 11, 2010


CERTIFIED MAIL


RETURN RECEIPT REQUESTED


In reply refer to Warning Letter SEA 10-11


Christopher T. Rangen, President Rangen, Inc. 115-13th Avenue South PO Box 706 Buhl, Idaho 83316


WARNING LETTER


Dear Mr. Rangen: On June 9-11, 2009, U.S. Food and Drug Administration (FDA) investigators inspected your animal feed manufacturing facilities located at 115-13th Avenue South, Buhl, Idaho. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Section 589.2000 (21 C.F.R. 589.2000), Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation, resulting in products being manufactured and distributed by your facility that were adulterated within the meaning of section 402(a)(4) of the Federal Food, Drug, and Cosmetic Act (the Act), 21 U.S.C. § 342(a)(4), and misbranded within the meaning of section 403(a)(1) of the Act, 21 U.S.C. § 343(a)(1). Our investigation determined that adulteration resulted from the failure of your firm to provide for measures to avoid commingling or cross-contamination. The adulterated feed was subsequently misbranded because it was not properly labeled. Specifically, we found:


1. Your firm failed to provide for and use cleanout procedures or other means adequate to prevent carry-over of products that contain or may contain proteins derived from mammalian tissues into animal feed that may be used for ruminants, as required by 21 CFR 589.2000(e)(1)(iii)(B). Since your feed is prepared, packed, or held under these conditions it is, therefore, adulterated under section 402(a)(4) of the Act, 21 U.S.C. § 342(a)(4).


• Mink feed that was not labeled "Do not feed to cattle or other ruminants," in accordance with 21 CFR 589.2000(e)(1)(i) and that, therefore, might be fed to ruminants, was produced using the same equipment as aquaculture feed that contains proteins derived from mammalian tissues, such as meat and bone meal. You conducted no clean-outs or flushes of equipment to remove proteins derived from mammalian tissues that may have been present before manufacturing the mink feed that might be fed to ruminants.


• The auger trucks you used to deliver bulk mink feed which contained or may have contained proteins derived from mammalian tissues were not subject to an effective clean-out prior to their use to deliver bulk animal feed, including ruminant feed, that did not contain such materials. There were no procedures to clean the trucks to remove proteins derived from mammalian tissues before shipment of animal feeds that did not contain such materials.


2. You failed to label all products which contained or may have contained proteins derived from mammalian tissues with the statement, "Do not feed to cattle or other ruminants," as required by 21 C.F.R. 589.2000(e)(1)(i). Such products are misbranded under Section 403(a)(1) of the Act, 21 U.S.C. § 343(a)(1). The misbranded product includes bulk mink feed.


• On June 9, 2009, the investigators observed approximately (b)(4) pallets of (b)(4) 50 pound bags of (b)(4) MINK FEED, lot 06/05/09. All bagged mink feed, as well as approximately (b)(4)% of bulk mink feed, manufactured at your facility, was produced using the aquaculture feed production equipment used to produce feed containing proteins derived from mammalian tissues. Because mink feed produced using this equipment may have contained mammalian tissues, it was not properly labeled, as required by 21 C.F.R. 589.2000(e)(1)(i).


This letter is not intended to serve as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct the above violations and you should establish a system whereby violations do not occur. Failure to promptly correct these violations may result in regulatory action, such seizure and/or injunction, without further notice.


We acknowledge your July 31, 2009 letter detailing procedures you had implemented or planned to implement to prevent future violations of FDA regulations relating to mammalian proteins in animal feed. In particular the letter stated that Rangen would no longer purchase meat and bone meal for use in any of its animal feeds and that existing inventories of mammalian protein ingredients would be exhausted by December 31, 2009. Division Manager, Joy Kinyon made similar assertions in the course of FDA's June 2009 inspection. The July 31, 2009 letter further set out procedures Rangen would use to remedy observed violations of FDA regulations while mammalian proteins were still being used at Rangen. Finally you explained steps taken to recover or relabel feed that may have been contaminated due to commingling resulting from your manufacturing and distribution procedures. Within fifteen (15) working days of receiving this letter you should, in writing, confirm the steps you took prior to receiving this letter and notify FDA of steps you have taken since receiving this letter to bring your firm into compliance with the law. Your response should include each step that has been taken or will be taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within fifteen (15) working days, state the reason for the delay and the time frame within which the corrections will be completed. Please include copies of any available documentation demonstrating that corrections have been made.


Your written reply should be directed to Scott A. Nabe, Compliance Officer, U.S. Food and Drug Administration, 22201 23rd Drive SE, Bothell, Washington 98021-4421. If you have any questions about this letter, please contact Mr. Nabe at (425) 483-4753.


Sincerely,


/s/


Charles M. Breen District Director Seattle District


cc: Joy A. Kinyon, Division Manager, Aquaculture Feeds-General Feeds Rangen, Inc. PO Box 706 115-13th Avenue South Buhl, Idaho 83316








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








Thursday, March 19, 2009


MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL






Friday, September 4, 2009


FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009






and all this was confirmed here ;




C O N F I R M E D




----- Original Message -----


From: "Terry S. Singeltary Sr."


To:


Sent: Thursday, November 05, 2009 9:25 PM


Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009






Thursday, November 12, 2009


BSE FEED RECALL Misbranding of product by partial label removal to hide original source of materials 2009






Tuesday, March 2, 2010


Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA






Monday, March 1, 2010


ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010






Monday, April 5, 2010


Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010






Saturday, July 23, 2011


CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE






Saturday, November 6, 2010


TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS


INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation






Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)


PRION DISEASE UPDATE 2010 (11)






the new BSE TSE PRION MAD COW risk category the OIE gave the USA, puts everyone around the globe at more risk of a tse prion mad cow type disease now.


in my opinion, this new risk category was bought and paid for by your local cattle dealer, via fraud.


IT is of my opinion, that the OIE and the USDA et al, are the soul reason, and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion diseases, including typical and atypical BSE, typical and atypical Scrapie, and all strains of CWD, and human TSE there from, spreading around the globe.


I have lost all confidence of this organization as a regulatory authority on animal disease, and consider it nothing more than a National Trading Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.


JUST because of low documented human body count with nvCJD and the long incubation periods, the lack of sound science being replaced by political and corporate science in relations with the fact that science has now linked some sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call for this organization to be dissolved. ...




IN A NUT SHELL ;


(Adopted by the International Committee of the OIE on 23 May 2006)


11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,






Thursday, May 30, 2013


World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease


U.S. gets top mad-cow rating from international group and risk further exposing the globe to the TSE prion mad cow type disease








Tuesday, June 4, 2013


INTERPRETING RESULTS OF FSIS VERIFICATION SAMPLING OF DOMESTIC BEEF PRODUCT DERIVED FROM ADVANCED MEAT RECOVERY SYSTEMS (AMR01/FAMR01) FSIS Notice 38-12






Thursday, February 14, 2013


The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease






Monday, June 3, 2013


Unsuccessful oral transmission of scrapie from British sheep to cattle






who is testing canine, feline, mink, for TSE in the USA ???




just kidding, we all know that no one is testing for the TSE prion in the feline, canine, or mink in the USA, there is no testing or surveillance efforts. kind of like the SSS policy of the USDA inc. with cattle, i.e. don’t look, don’t find, problem solved $$$


I can assure you, the problem is not solved. ...


Tuesday, March 05, 2013


A closer look at prion strains Characterization and important implications Prion


7:2, 99–108; March/April 2013; © 2013 Landes Bioscience






Monday, April 15, 2013


Dr. Stephen B. Thacker Director Centers for Disease Control and Prevention′s Office of Science, Epidemiology and Laboratory Services (OSELS) dies from Creutzfeldt Jakob Disease CJD






Sunday, February 10, 2013


Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection report/CJD






Tuesday, May 28, 2013


Late-in-life surgery associated with Creutzfeldt-Jakob disease: a methodological outline for evidence-based guidance








TSS

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