smalltime said:
I am asumming flounder you are against that type of control because the cats and wolves will get prion desease and then spread it to other spieses?
that's my take, the threat is real, and in the end, it's not going to control anything, other than enhance the exposure of the TSE prion agent. if you must reduce the herd, then shoot them, test them (wait for results), and then eat them.
it's been documented that cats can easily become infected with the TSE prion disease. in fact, a study out last year about cwd to domestic cats ;
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
[email protected]
Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
Hunting and diet
A successful generalist predator, the cougar will eat any animal it can catch, from insects to large ungulates (over 500 kg). Like all cats, it is an obligate carnivore, feeding only on meat. The mean weight of vertebrate prey (MWVP) was positively correlated (r=0.875) with puma body weight and inversely correlated (r=-0.836) with food niche breadth in all America. In general, MWVP was lower in areas closer to the Equator.[3] Its most important prey species are various deer species, particularly in North America; mule deer, white-tailed deer, elk, and even large moose are taken by the cat. Other species such as Bighorn Sheep, wild horses of Arizona, domestic horses, and domestic livestock such as cattle and sheep are also primary food bases in many areas.[38] A survey of North America research found 68% of prey items were ungulates, especially deer. Only the Florida Panther showed variation, often preferring feral hogs and armadillos.[3]
Shown eating. Cougars are ambush predators, feeding mostly on deer and other mammals. Investigation in Yellowstone National Park showed that elk, followed by mule deer, were the cougar's primary targets; the prey base is shared with the park's gray wolves, with whom the cougar competes for resources.[39] Another study on winter kills (November–April) in Alberta showed that ungulates accounted for greater than 99% of the cougar diet. Learned, individual prey recognition was observed, as some cougars rarely killed bighorn sheep, while others relied heavily on the species.[40]
http://en.wikipedia.org/wiki/Cougar
Oral.22:
Transmission and Pathogenesis of Chronic Wasting Disease in Cervid and Non-Cervid Species
Edward Hoover,† Candace K. Mathiason, Nicholas J. Haley, Timothy D. Kurt, Davis M. Seelig, Amy V. Nalls, Mark D. Zabel, Glenn C. Telling Department of Microbiology, Immunology, and Pathology; Colorado State University; Fort Collins, CO; Department of Microbiology, Immunology and Molecular Genetics and Neurology; University of Kentucky Medical Center; Lexington, KY USA †Presenting author
Now recognized in 18 states in the US, two Canadian provinces, and one Asian country, efficient horizontal transmission is a signature trait of chronic wasting disease (CWD) of cervids. The facile spread of CWD appears linked to the prion/host relationship facilitating efficient mucosal uptake, peripheral lymphoreticular amplification, and horizontal dissemination exploiting excretory tissues and their products. In addition, recent studies suggest the likelihood of early life mother to offspring transmission. Growing evidence from studies of cervid CWD exposure by natural routes indicate that the incubation period for overt infection detection and disease onset (if any) may be much longer than originally thought. Whether non-cervid species (including humans) may be susceptible to CWD infection and/or act as reservoirs for infection in nature remains unknown. In vitro and in vivo studies of the CWD species barrier indicate the potential for a host range extending beyond cervid species, although no evidence for this has thus far been detected in nature. Interestingly, rodent and mustelid species sympatric with free ranging cervids have been shown susceptible to CWD prions and such trans-species infection broadens the host range/strain characteristics of CWD prions. While the origins of CWD remain unknown, the relationship between sheep scrapie and CWD and the existence of multiple CWD prion strains/quasispecies remain interesting and merit further investigation.
snip...more here ;
Monday, August 8, 2011
Susceptibility of Domestic Cats to CWD Infection
Oral.29: Susceptibility of Domestic Cats to CWD Infection
http://felinespongiformencephalopathyfse.blogspot.com/
now, canine spongiform encephalopathy has never been documented to date. however, like the bungling brains episode of the sheep and cattle in the UK, something similar happened in the 'hound study'. you can take this with how ever many grains of salt you wish, but something was fishy about those hound brains ;
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...
http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
NEW URL ;
http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
76 pages on hound study;
http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf
NEW URL ;
http://web.archive.org/web/20030327022236/http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf
I thought that in Britain dogs had contracted BSE, but perhaps not?
not so fast here;
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).
http://www.bseinquiry.gov.uk/witness/htm/stat067.htm
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.
snip...
http://www.bseinquiry.gov.uk/files/ws/s324.pdf
NEW URL ;
http://collections.europarchive.org/tna/20080102174910/http://www.bseinquiry.gov.uk/files/ws/s324.pdf
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
critical. For more details see- http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf
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
===============end...tss==============
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
http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf
NEW URL ;
http://collections.europarchive.org/tna/20081106102318/http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf
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.
http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf
NEW URL ;
http://collections.europarchive.org/tna/20080103034308/http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf
37. Putative TSE in hounds - work started 1990 -(see para 41)
Robert Higgins, a Veterinary Investigation Officer at Thirsk, had been working on a hound survey in 1990. Gerald Wells and I myself received histological sections from this survey along with the accompanying letter (YB90/11.28/1.1) dated November 1990. This letter details spongiform changes found in brains from hunt hounds failing to keep up with the rest of the pack, along with the results of SAF extractions from fresh brain material from these same animals. SAFs were not found in brains unless spongiform changes were also present. 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).
http://www.bseinquiry.gov.uk/witness/htm/stat067.htm
1. I have had no further submission of material or communication regarding this survey since January 1991.
http://www.bseinquiry.gov.uk/files/yb/1991/10/17001001.pdf
NEW URL ;
http://collections.europarchive.org/tna/20080103024918/http://www.bseinquiry.gov.uk/files/yb/1991/10/17001001.pdf
HOUND SURVEY PATHOLOGICAL REPORT (see positive results)
http://www.bseinquiry.gov.uk/files/yb/1990/11/28001001.pdf
NEW URL ;
http://web.archive.org/web/20030605233318/http://www.bseinquiry.gov.uk/files/yb/1990/11/28001001.pdf
kind regards, terry
###########bse-l ############
http://caninespongiformencephalopathy.blogspot.com/
5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man.
***********************
***I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.***
************************
6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.
R. Bradley
23 September 1990
CVO (+Mr Wells' comments)
Dr T W A Little
Dr B J Shreeve
90/9.23/1.1.
http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
2012
"which may prompt a reevaluation of the effectiveness of species barriers"
Thursday, January 26, 2012
The Risk of Prion Zoonoses
Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167
http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html
http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html
now, what have we been feeding cats and dogs ???
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html
Thursday, September 3, 2009
429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
http://madcowfeed.blogspot.com/2009/09/429128-lbs-feed-for-ruminant-animals.html
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
http://madcowfeed.blogspot.com/2009_09_01_archive.html
Tuesday, November 3, 2009
re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009
http://madcowfeed.blogspot.com/2009/11/re-foia-request-on-feed-recall-product.html
From: Terry S. Singeltary Sr.
To:
[email protected]
Cc:
[email protected] ;
[email protected] ;
[email protected] ;
[email protected].
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
September 4, 2009
TO:
Food and Drug Administration
Division of Freedom of Information (HFI-35)
Office of Shared Services
Office of Public Information and Library Services
5600 Fishers Lane
Rockville, MD 20857
Or requests may be sent via fax to: fax number 301-443-1726 or 301-443-1719. If experience difficulty sending a fax, please call (301) 443-2414.
FROM:
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
Greetings FDA FOIE, and the Honorable Phyllis Fong et al @ OIG FOIA,
ANOTHER FOIA REQUEST PLEASE !
I apologize for wasting your time. this could have been handled differently if the FDA et al would just clearly identify these feed recalls with exactly what was in them, and what type recall it is.
I was told that the only way to find any more information on the following recall, i would have to submit a FOIA ? why, i do not know ?
----- Original Message -----
From: Pritchett, Burt
To: Terry S. Singeltary Sr.
Sent: Thursday, August 27, 2009 3:26 PM
Subject: RE: hello Mr. Pritchett Sir !!! mad cow feed question
Terry,
That is the extent of the public information on the recall. If you wish to obtain additional information, you should submit a freedom of information act request through our communications staff. You could send an email request to:
[email protected]
Burt
================end...TSS
Greetings again FDA, OIG et al,
I am trying to find out more information on another recall, that contains possible mad cow protein? but we do not know for sure, the way the recall warning letters are being wrote up now.
I had to file FOIA last week for the same thing. see ;
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html
and I recieved 'confirmation' of my request in the postal mail with Log No. xx-xxxxx.
HOWEVER, SADLY, I requested another explaination again from Pritchett, Burt on this newest suspect mad cow feed recall this week below, explaining to him that this is rediculous to have to file a FOIA on every feed recall now, and that all he had to do was to explain exactly what we are speaking of in these recalls, and I have gotten no response to date. SO, I will continue to write these FOIA request, until we get this straightened out, even if it takes another 6+ years to find the truth.
F.O.I.A request on the following please ;
PRODUCT Bulk ground corn; distributed by Saginaw Flakes, Saginaw, TX, Recall # V-258-2009
CODE Bulk ground corn shipped between 05/13/-14/09
RECALLING FIRM/MANUFACTURER Recalling Firm: Fargam Land & Grain, Saginaw, TX, by telephone on May 21, 2009. Manufacturer: Mars Petcare US, Clinton, OK.
Firm initiated recall is ongoing.
REASON Bulk ground corn used as feed for ruminant animals may have been contaminated with prohibited material.
VOLUME OF PRODUCT IN COMMERCE 429,128 lbs.
DISTRIBUTION TX, LA
END OF ENFORCEMENT REPORT FOR SEPTEMBER 2, 2009
###
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm181251.htm
IS this is a BSE/TSE feed ban violation of some sort, or exactly what ?
NOT KNOWING EXACTLY what this recall is about, we must assume it is just more mad cow feed in commerce, but they refuse to tell us exactly what it is.
ruminant animals may have been contaminated with prohibited material
exactly what was it ???
under regs just previously posted, if i understand this right, you now have 3
Subpart B-Listing of Specific Substances Prohibited From Use in Animal Food or Feed ;
§ 589.1000 Gentian violet.
§ 589.1001 Propylene glycol in or on cat food.
§ 589.2000 Animal proteins prohibited in ruminant feed.
http://ecfr.gpoaccess.gov/cgi/t/text/text-idx?c=ecfr&sid=8f6d4f71330c3337921d820e1854476e&rgn=div5&view=text&node=21:6.0.1.1.26&idno=21
SO, which one is it ???
THIS recall is not confusing ;
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
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
NEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
snip...full text ;
http://caninespongiformencephalopathy.blogspot.com/
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
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
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>
Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/direct.php?id=20101206.4364
October 2009 O.11.3 Infectivity in skeletal muscle of BASE-infected cattle
Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy
Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.
Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.
Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.
Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
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