Hello,
xxxxxxxxx wrote ;
In my opinion based on empirical evidence it appears that world fish depletion has led to higher cost of fish and feed meal producers subsequently turning to abattoirs to buy lower cost meat offal to produce meat meal in place of fish meal.
Meat meal fed to cattle apparently brought brain matter and the relevant Prion protein of the same species together, leading to BSE in that species and CJD in humans.
Concerning similar disease and links between offal and feed I have recently noticed imported dry-pellett dog food in Australia and I now wonder if poddy lambs or goats around homesteads and dog food, might be linked to a Prion protein transfer that is presently unseen. ...END
========================
Thursday, October 7, 2010
Australia first documented case of atypical scrapie confirmed
First occurrence of atypical scrapie
http://nor-98.blogspot.com/2010/10/australia-first-documented-case-of.html
xxxx, you bring up some very valid points of concern. Just recently, this year, we learn that indeed here in the USA, dog and cat food i.e. pet food, it is still legal to feed banned rumminant mad cow feed, and you will see from this recent mad cow feed warning letter i had to finally request to get via the F.O.I.A., you will see just how much risk factor there is from these feeds being exported out of the USA to unsuspecting countries around the Globe, as we have seen recently too with the list of banned products that continued to be exported to Australia from the USA. Also, even though there is no _documented_ case of canine spongiform encephalopathy, don't bet your last dollar that it has not happend.
OF course, we could argue till the mad cows come home about the infamous ''spontaneous" hypothesis for everything prion that has no route our source identified to date, but it would do no good, fact is, is, it can't be proven yet with current scientific resources. but, I will say this, IF ''spontaneous'' TSE of any form is ever proven in the field, naturally, then that will be everyone's worst nightmare due to the ramifications there from i.e. the pass it forward mode of many routes and sources. you see, you could never eliminate the source from a spontaneous event. YOU could ban everything, everyone could be in compliant, and the one spontaneous event would then slip by and be rendered unto thee, for all to eat, or be exposed to there from. FROM THAT POINT FORWARD, mandatory 100% testing across the board would then be the only rational/sensible/logical/humane/scientific thing to do, to further prevent exposure. OF course, we know how any of the above 'rational/sensible/logical/humane/scientific' plays into the world of TSE Science, TRADE, and the almighty dollar goes. all that goes right out the window.
The studies below will show that it has probably already happened, as with the Feline Spongiform Encephalopathy. I would like to keep this short, but when supplying science with debate, it's just not possible, and I like for everyone to see the science, to date. It's all too long to post here, so I just blogged it all and for those interested, they can go there and read the science. ...
kind regards,
terry
• 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).
snip...
Monday, March 8, 2010 UPDATE 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009 Greetings,
I got a follow on this in the mail this past Saturday in the mail. thought some might be interested in the following ;
DEPARTMENT OF HEALTH & HUMAN SERVICES Public Health Service Food and Drug Administration Rockville MD 20857
Terry Singeltary P.O. box 42. Bacliff, TX USA 77518
Dear Requestor
In reply refer to: F2009-7430
This is in response to your Freedom of Information Act (FOIA) request received by the Food and Drug Administration (FDA) on September 10,2009 which you ask for Recall V-258-2009. I apologize for the delay in our response to you. Enclosed you will find the records you requested. The following charges will be included in a monthly invoice:
Reproduction Search Review Total 5 Pages hour $.50 $ $.50
The above charges may not reflect final charges for this request. Please DO NOT send any payment until you receive an invoice from the Agency's Freedom of Information Staff (HFI-35).
Sincerely yours,
Sandy McGeehan Paralegal Specialist Communications Staff Center for Veterinary Medicine
Memorandum
Date August 26, 2009
From CVM Animal Health Hazard Evaluation Committee
Subject Problem:
Fargam Land & Grain recalled 429,128 pounds of ground corn because it may have been contaminated with prohibited material (material prohibited for use in ruminant feed by the 1997 BSE feed regulation) and was not labeled with the cautionary statement.
The feed mill received two semi trailer loads of barley that had been recalled by Mars Petcare US because it had been contaminated by dog food, some of which is formulated to contain bovine origin meat and bone meal.
The auger used to receive the barley was used to receive two truck loads of corn before the feed mill became aware of the problem with the barley. This potentially allowed some of the dog food in the barley to be carried over into the corn.
Recall Event IDIRES #: 52103
DAF/Surveillance #: 09234
CVM Recall and Emergency Coordinator (Kathy Hemming-Thompson), HFV -234
Field/RES Report Data:
Recalling firm: Fargam Land & Grain 505 Burlington Rd Saginaw, TX 76179
Manufacturer: Mars Petcare US 1 Doane Rd Clinton, OK 73601
Product & Code: Bulk ground corn; 70AY -02
Quantity Manufactured: 429,128 pounds
Quantity Distributed: 429,128 pounds
Recall Contact: Phil Farr, Owner, Fargam Land & Grain, Saginaw, TX
FDA District: Dallas
Field Recommended Classification: Class III
Effectiveness Check Level: Direct Accounts
Page 2 of 4 - DAF 09234 - Health Hazard Evaluation
Background: The firm is a feed mill that stores and manufactures products intended for use in animal feed. Its business is commingled with Saginaw Flakes, a feed mill which is under the same ownership, and located across the street from Fargam Land & Grain. A limited inspection was conducted to determine compliance with CP 7371.009 after the firm notified the Office of the Texas State Chemist that it had received four semi trailer loads of barley that may have contained dog food.
ReView:
please see full text ;
http://madcowfeed.blogspot.com/2010/03/update-429128-lbs-feed-for-ruminant.html
Monday, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
Greetings, Another Big Myth about Transmissible Spongiform Encephalopathy, is that TSE will not transmit to dogs. This is simply NOT TRUE. IT is perfectly legal to feed dogs and cats here in the USA bovine meat and bone meal. Canine dementia is real. how many dogs and cats here in the USA are tested for mad cow disease ? I just received this F.O.I.A. request, and thought I would post it here with a follow up on MAD DOG DISEASE. This is a follow up with additional data I just received on a FOIA request in 2009 ; see full text, and be sure to read the BSE Inquiry documents toward the bottom ;
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://collections.europarchive.org/tna/20080102174910/http://www.bseinquiry.gov.uk/files/ws/s324.pdf
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-
SEE UPDATE URL HERE ;
http://web.archive.org/web/20030327015011/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
Agenda Item 7 - Any Other Business: the Hounds Survey 26.
Paper SEAC 19n responded to a request from the Committee for a re- evaluation of the pathology material in the hounds survey to determine whether anything further could be derived from the available data. 27.
In discussion of the options for further work set but in the paper most members felt that the study had been badly carried out and there would be little value in spending more money to try and improve the interpretation of the data. It was particularly significant that no clinical data were available, although the Committee were reminded that most of the hounds were clinically normal culls. Dr Kimberlin was concerned about the lack of results from the study. Any further work would . require a control but this could be obtained by exposing hounds to BSE which would also help to answer questions about species sensitivity, thereby serving more than one purpose. The use of immunocytochemistry was fairly robust and would enable the work to be brought to a satisfactory conclusion. Dr Kimberlin's view that this would be necessary was confirmed by an article, circulated at the meeting, showing that the predictive protein sequence was the same in dogs as in cattle. Mr Eddy noted that such an experiment could be expensive and it would be necessary to know what questions were to be addressed. 28.
Concluding, Dr Tyrrell said that there was a range of opinions in the Committee from those who thought further work a waste of time to those who wished to do limitedfurther experiments using immunocytochemistry. The Committee did not suggest transmission studies and thought that the lack of clinical data was a major weakness. Hounds were initially studied on the recommendation of the Southwood Committee because they were perceived as a "high risk" population exposed to large quantities of potentially infective bovine tissues. Since then, however, a range of other species had been identified with TSEs, and the study of hounds was therefore less critical.
http://web.archive.org/web/20030327015011/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
======================================
http://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html
TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS
TSE in hounds
Tue, 8 Aug 2000 BSE Inquiry document YB90/11.28/1.1 obtained by Terry S. Singeltary Sr.
37.Putative TSE in Hounds - work started 1990
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 [scrapie-associated fibrils] 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.
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.
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 in cats and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.
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.
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.
Opinion (webmaster): It was politically unacceptable to find TSE in dogs. However, hunting dogs in particular received horrific exposure to terminal downer BSE cows, including skull and spinal column. The most interesting aspect is that hound ataxia, taken above as a proxy for dog TSE, goes back to the 1930's, the time of the louping ill vaccine accident causing tens of thousands of sheep to develop scrapie. Some of the dog cases could be due in fact to consumption of sheep scrapie.
http://www.mad-cow.org/00/aug00_late_news.html#ggg
HOUND STUDY
The interpretation of these cases is therefore limited to suggesting that there is no evidence of a florid scrapie-like encephalopathy as has presented in domestic cats.
THERE are nevertheless observations, including in some cases localized vacuolar changes, the significance of which has not been determined.
The objective to he hound survey is stated to be detection of spongiform changes in brains of hounds. THIS would seem to have been ACHIEVED but the design of the survey, without established diagnostic methods for a scrapie-like encephalopathy presenting in dogs, prevents interpretation of the significance of the changes.
ALSO, the changes which have given rise to referral of cases seem to have occurred with relative frequency in the survey to date. This being so it can be anticipated that a significant proportion of the survey could result in unresolved cases.
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://collections.europarchive.org/tna/20081106031419/http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
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://web.archive.org/web/20030326184703/www.bseinquiry.gov.uk/files/ws/s067.pdf
http://web.archive.org/web/20030327010655/www.bseinquiry.gov.uk/files/ws/s067x.pdf
NOW, with all that said, let's look at the uptake of the PrP in feed to some fish, and just a few examples of mad cow fish feed in commerce ;
Wednesday, April 02, 2008
In vivo prion protein intestinal uptake in fish
1: APMIS. 2008 Mar;116(3):173-80.
In vivo prion protein intestinal uptake in fish.
Dalla Valle AZ, Iriti M, Faoro F, Berti C, Ciappellano S. Department of Food Science and Microbiology (DISTAM), Section of Human Nutrition, University of Milan, Milan, Italy.
Intestinal uptake of abnormal prion protein (PrP(Sc)), the pathological agent involved in transmissible spongiform encephalopathies (TSEs), has been investigated in rainbow trout (Oncorhynchus mykiss). Experimental procedures were conducted in vivo by immunohistological PrP(Sc) localization in intestine and pyloric caeca after forced feeding of infected material. Results indicate that PrP(Sc) was absorbed by the intestinal mucosa and that it persisted in the fish gastrointestinal tract for up to 3 days in pyloric caeca and for up to 7 days in the distal intestine. It did not remain longer than 15 days in the fish intestine; furthermore, it did not cross the intestinal barrier.
PMID: 18377582 [PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/18377582?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Studies of the transmissibility of BSE to fish :
Experimental Transmission
Groups of Trout and Sea Bream (Spaurus aurata L.) were fed or were inoculated i.c with BSE affected bovine material. Approx. 40 experimental and 15 control in each group. Abnormally swimming animals sacrificed and brains dissected. Samples (brain, muscle, spleen, liver, intestine, reproductive organs, eye, kidney) taken 1, 2, 15, 30, 60, 90, 120 days pi. No abnormal swimming between 1 to 120 days. No evidence of infection by histology, IHC or Western blot (prionics). Histological findings: No evidence of significant changes in the brains or other organs studied from fish sampled at 1, 2, 15, 30, 60, 90 and 120 days pi.
Immunohistochemical findings: by using ABC-peroxidase technique with mAbs 2A11 and 6H4, no evidence of PrPres deposition has been detected in any sample. The effectiveness of McAb 2A11 on bovine and murine prion infected brains was previously verified with ABC-peroxidase technique, and immunohistochemistry with 6H4 was performed as described previously. However, in the absence of positive TSE infected fish controls and the uncertainty of the existence of a molecule in fish equivalent to mammalian PrP, the efficacy of these antibodies for detection of any surrogate marker for TSE infectivity in fish is unknown. Western blot technique: by using the “Prionics test” (mAb 6H4), every sample of all the groups were negative to the presence of proteinase-K resistant prion protein.
It must be remembered that the present period of observation (4 months) is probably not sufficient to provide evidence that would make distinction between residual inoculum infectivity and pathogenetic amplification of agent. In a further experimental step the project proposes to evaluate the possible transmission of prions (Scrapie and BSE) to different fish species (Sea Bream, Sea Bass (Dicentrarchus labrax L.) and Trout). The ultimate test would be to feed back/inoculate material from fish experimentally challenged into more fish of the same species. This should be considered.
http://europa.eu.int/comm/food/fs/sc/ssc/out320_en.pdf
http://madcowfeed.blogspot.com/2009/06/farmed-fish-may-pose-risk-for-mad-cow.html
From: TSS (216-119-162-76.ipset44.wt.net)
Subject: Attempted transmission of TSE to fish from ovines and bovines:
''Infectivity was also found to persist sporadically in the intestine of fish''
Date: March 18, 2003 at 12:23 pm PST
Subject: RE-High Country eNewsletter 3-18-03
Date: Tue, 18 Mar 2003 13:32:59 -0600
From: "Terry S. Singeltary Sr."
To: plarmer@hcn.org
CC: RayRing@hcn.org, emarston@hcn.org, jess@hcn.org
And as Rebecca Clarren writes, there are far greater differences between farmed and wild salmon than just a floating fish pen. In "Are you gonna eat that?", Clarren looks at the hidden dangers of farmed salmon, including cancer-causing PCBs, antibiotics, and a color additive called canthaxanthin, which may cause vision problems.
snip...
We laugh, but it’s easy to see the results of similar unconscious choices of the past: The great bison herds that once roared across the Plains are gone, and in their place we have industrial cattle feedlots. Now, with the advent of fish farms, we’re seeing the same wholesale replacement of creation with industrialized food production. This is a dangerous illusion: that we can enjoy the bounty of nature without protecting rivers, streams and landscapes.
Is the nation ready to really look at what’s on the end of its fork? At this point, it’s all up in the air — like the salmon at the Pike Street Market. The difference is, this is not a game of catch that consumers should watch from the sidelines.
http://www.hcn.org/servlets/hcn.Article?article_id=13807
WARNING LETTER
June 12, 2001
Mr. Scott Nelson, Owner Integral Fish Foods, Inc. 715 South 7th Street Grand Junction, CO 81501
Ref. #: DEN-01-35
Dear Mr. Nelson,
An inspection of your fish feed manufacturing operation located at Grand Junction, Colorado, conducted by a Colorado Department of Agriculture Inspector on March 20, 2001, 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 and/or distributed by your facility to be adulterated within the meaning of section 402(a)(4) and misbranded within the meaning of Section 403(f) of the Federal Food, Drug, and Cosmetic Act (the Act).
The inspection found that your procedures to prevent cross-contamination are inadequate in that:
You do not have written procedures specifying the clean-out procedures for your feed mixer.
Our investigation also found that you fail to label your products, Fat Cat Catfish Fingerling Feed and Gold Nugget Trout Fry Feed #2 Crumble, each containing meat and bone meal, with the required cautionary statement "Do Not Feed to Cattle or Other Ruminants". The FDA suggests 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.
The above is not intended to be an all-inclusive list of violations. As a manufacturer of materials intended for animal feed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. We have enclosed a copy of the FDA's Small Entity Compliance Guide to assist you with complying with the regulations.
Page 2 - Integral Fish Foods, Inc. June 12, 2001
We find it quite disturbing that the above violations STILL EXIST CONSIDERING YOU HAVE BEEN ADVISED ON 2 PREVIOUS OCCASIONS OF THESE REQUIREMENTS, INCLUDING APRIL 7, 1999 and MARCH 6, 2000....end...TSS
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
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
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
PRODUCT a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006
RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT.
Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
SSC meeting of 16-17 January 2003 / 2
Agenda 01_03.doc
Draft agenda of the Scientific Steering Committee Meeting of 16-17 January 2003
1. Welcome, apologies, introductory remarks, declaration of interest.
2. Approval of the agenda
3. Approval of the minutes of the meeting of 5-6 December 2002.
4. Procedural matters (if any) - Information on EFSA and the current transitional stage.
5. Multidisciplinary matters:
a. Co-ordination: Reports of the Chairmen of the 8 Scientific Committees;
b. Harmonisation of risk assessment methods: - Progress report on Task Force activities; - Report on the feedback received on the public consultations;
c. Emerging scientific issues.
d. Guidance document on the information needed for the risk assessment of genetically modified plants and derived food and feed.
6. Multidisciplinary matters relating to TSE/BSE
6.1. Report by the chairman of the TSE/BSE ad-hoc group meeting of 9 January 2003
6.2. Reports on specific multidisciplinary matters relating to TSE/BSE: a. Geographical BSE Risk: the GBR of certain countries. b. Update of the SSC opinion on the safety of di- and tricalcium phosphate from bones;
c. Quantitative assessment of the risk of tallow, gelatine and dicalcium phosphate;
d. BSE risk of the bovine autonomic nervous system;
e. Potential risks arising from the use of small incinerators;
f. Conditions under which (1) safe burial and (2) safe burning can be achieved (progress report)
g. Chronic Wasting Disease.
h. BSE cases born after the reinforced feed ban in the UK (BARBs)
i. BSE-related culling in cattle.
j. The feeding of wild fishmeal to farmed fish and recycling of fish with regard to the risk of TSE.
k. Rapid tests: Information
7. Information on the follow-up given to the opinions adopted at previous SSC meetings.
8. Information by the Commission services on other matters related to consumer health.
9. Any other business.
http://europa.eu.int/comm/food/fs/sc/ssc/agenda/agenda12_en.pdf
F:\WebDev\TSE in fish_OPINION_0303_FINAL.doc
EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Scientific Steering Committee
OPINION ON :
THE FEEDING OF WILD FISHMEAL TO FARMED FISH AND RECYCLING OF FISH WITH REGARD TO THE RISK OF TSE
ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 6-7 MARCH 2003.
F:\WebDev\TSE in fish_OPINION_0303_FINAL.doc 1
THE FEEDING OF WILD FISHMEAL TO FARMED FISH AND RECYCLING OF FISH WITH REGARD TO THE RISK OF TSE
OPINION
MANDATE:
Mammalian MBM and other mammalian products have historically been fed to farmed fish. Furthermore, intra-species and intra-order recycling via feed is common practice in fish farming. It is therefore important to address the question whether the latter practice could enable mammalian TSE agents to establish themselves in fish and for species adaptation of such agents to occur. This could lead to the development of a TSE in fish that might lead to a TSE epidemic in fish and/or create a health risk for the consumer. The outcome of the assessment would improve the scientific basis for the possible updating of the animal waste disposal legislation and other legislative texts in the field of veterinary public health. The Scientific Steering Committee (SSC) was therefore invited:
(1) to advise whether the feeding of wild fishmeal to farmed fish presents any risk to animal or human health vis-à-vis TSE’s;
(2) if appropriate, to suggest examples of conditions under which intra-species or intra-order recycling of fish could be allowed. The SSC asked the TSE/BSE ad hoc Group to prepare a scientific report to serve as basis for an opinion on the two questions. The report, finalized by the TSE/BSE ad hoc Group at its meeting of 5 September 2002, is attached. This report is largely based on various SSC opinions and reports of the TSE/BSE ad hoc group related to animal waste disposal and intraspecies recycling, on elements from the (draft) report of the Scientific Committee on Animal Health and Welfare on “The use of fish waste in aquaculture” and on the interim results of the FAIR CT97 3308 project entitled “Separation, identification and characterization of the normal and abnormal isoforms of prion protein from normal and experimentally infected fish”
BACKGROUND:
1. Very little is known about the possible occurrence of TSEs in fish. No targeted (epidemiological) surveys have been conducted to detect pathological changes in fish consistent with TSEs. Limited research results currently available are inconclusive regarding whether or not TSE agents from other orders (e.g. mammals) can be transmitted to fish and lead to replication and disease, or whether or not (certain) fish species could generate or support TSE agent replication based upon the existence of a piscine prionprotein molecule.. However, these possibilities cannot be totally excluded as recently a homologue to prion-protein was identified in the pufferfish Fugu rubripes, showing high homology with mammalian PrP sequences and in another publication the normal isoform of amyloid protein (PrP) was identified in brains of spawning salmon. On the other hand, intra-species and intra-order “recycling” of fish materials occurs naturally in most if not all fish environments. It is likely that natural predation would offer limited scope for amplification of the agent and the “infectivity" could remain confined to a small number of the sea or freshwater fish or mammals. This principle may, however, not apply if the TSE agent were external to the fish environment/ecosystem and it is therefore justified to avoid the introduction of such agents to the fish environment, as this could possibly result in fish presenting a risk to other animal or human health vis-à-vis TSE’s. At this stage of knowledge the SSC, can only assume that the same biological rules that apply to mammalians might apply to fish. This is probably the best one can presently achieve, awaiting the results of current research and the realisation of the urgent requirement for further research to be carried out.
2. It is further appropriate to highlight the following additional uncertainties that result from such an approach:
- Unknowns exist regarding the structures of putitive fish PrP’s and how they might compare with the structures of mammalian PrP’s. Homologies between them would influence the magnitude of the species/order barrier (e.g., transmission of BSE from cattle to fish).
- Strictly speaking, intra-species recycling refers to the recycling of one given animal species to the same species, for example trout to trout. If fish-meals fed to a given species have been derived from a mixture of various / different fish species, it would be more appropriate to use the term “intra-order” recycling. In this case the level of the barrier is likely to be higher than in case of intra-species recycling, assuming that this is determined in fish by the PrP gene sequence and that there is a natural variation in the sequence between fish species. In practice there is the potential for a mixture of both types of recycling to occur.
- If TSEs were naturally present in fish populations, they may not manifest themselves in the same way as the known TSEs of mammalian species or may even not be recognised as a disease entity.
OPINION:
1. The risks caused by recycling in general, are addressed in the SSC opinion of 17 September 1999 on Intra-Species Recycling - the risk born by recycling animal byproducts as feed with regard to propagating TSE in non-ruminant farmed animals.
2. From the limited available research results, scientific literature on TSE’s in fish and routine examinations of fish brain in the course of fish disease diagnosis, it can be concluded that there is no evidence that a natural TSE exists in fish and that there are no indications of replication of scrapie or BSE agent in experimental transmission studies.
On the question whether the feeding of wild fishmeal to farmed fish presents any risk to animal or human health vis-à-vis TSE’s, the SSC therefore concludes that there is currently no evidence of any such risk existing. The data from the transmission experiments in the above-mentioned FAIR project and from other sources are still very limited and incomplete. Only three species of fish (Trout, Turbot and Sea Bream) are included in the experiments and no marine mammals, which could be more susceptible to TSE’s than fish, have been studied so far in this respect. Therefore, as always, ongoing research should be monitored closely to permit a possible update of this conclusion should research results call for such update.
3. Some theoretical risks could exist, linked to feeding possibly TSE-contaminated feeds to animals currently believed to be not susceptible, including fish. These risks include the possible build-up of a pool of infectivity in animals that do not develop disease but may potentially be able to harbour the agent as residual infectivity in the digestive system and/or replicate the agent. The latter risk is higher when intra-species recycling is practised due to the absence of a species barrier. Also the risk of adaptation of the agent to hitherto non-susceptible hosts should be considered. Regarding the request to, if appropriate, suggest examples of conditions under which intra-species or intra-order recycling of fish could be allowed, the SSC therefore considers in general that potentially TSE infected feed should not be fed to fish and that sourcing of fish by-products (including for their use in fish-derived feed) should not be performed from fish that have been exposed to potentially infected feed.
4. With regard to the appropriate treatment of fish materials, the SSC refers to its opinion of June 1999 on “Fallen stock”1 and to the Report of the Scientific Committee on Animal Health and Animal Welfare on “The use of fish by-products in aquaculture” adopted on 26 February 2003. 1 Scientific Opinion on The risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials.
Adopted By the Scientific Steering Committee at its meeting of 24-25 June 1999.
REPORT ON THE FEEDING OF WILD FISHMEAL TO FARMED FISH AND RECYCLING OF FISH WITH REGARD TO THE RISK OF TSE.
Rapporteur: Dr E. Vanopdenbosch
I. MANDATE
Intra-species or intra-order recycling is common practice in fish and it is thus justified to address the theoretical risk that such recycling could lead, for example, to the adaptation of TSE agents to certain fish species and/or the building up of an infectivity pool which could create a health risk for the consumer and/or to a TSE epidemic in fish. The outcome of the assessment would improve the scientific basis for the possible updating of the animal waste disposal legislation and other legislative texts in the field of veterinary public health. The Scientific Steering Committee (SSC) was therefore invited:
(1) to advise whether the feeding of wild fishmeal to farmed fish presents any risk to animal or human health vis-à-vis TSE’s;
(2) if appropriate, to suggest examples of conditions under which intra-species or intra-order recycling of fish could be allowed. A scientific report to serve as basis for an opinion on the two questions was prepared under the rapporteurship of Dr. E. Vanopdenbosch and with inputs from Prof. C.L.Bolis, Prof.Em.B.Lahlou, Dr.P.Brown, Dr.R.Bradley, Dr.Ph.Poujeol, Prof.Dr.D.Dormont, Dr.C.Ducrot and Dr.G.Wells. The report was finalised by the TSE/BSE ad hoc Group at its meeting of 5 September 2002.
2. PRELIMINARY REMARK
The current report is largely based on the following documents:
- SSC Opinion (EC, 1999a) on the risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials.
- SCC Opinion (EC, 1999b) the risk born by recycling animal by-products as feed with regard to propagating TSE in non-ruminant farmed animals.
- SSC Opinion (EC, 2000) on the Scientific basis for import bans proposed by 3 member states with regard to BSE risks in France and the Republic of Ireland; on the Scientific basis for several measures proposed by France with regard to BSE risks and on the Scientific basis for banning animal protein from feed for all farmed animals, including pig, poultry, fish and pet animals.
- Interim results (2002) of the FAIR CT97 3308 project entitled “Separation, identification and characterisation of the normal and abnormal isoforms of prion protein from normal and experimentally infected fish”
- Scientific Committee on Animal Health and Animal Welfare (2002). Draft
report on “The use of fish waste in aquaculture.”
3. FEEDING OF FARMED FISH
(See also the Report of the Scientific Committee on Animal Health and Animal Welfare on “The use of fish by-products in aquaculture” adopted on 26 February 2003.)
Since the end of the Second World War, the rate of growth of marine fisheries has been consistently somewhat higher than the rate of growth of the world's human populations. It has therefore been much higher than the rate of growth of agricultural food production. In fact, since the 1950's, practically each year's world fish catch has set a new record. Aquaculture is defined as the farming of aquatic organisms including fish, molluscs, crustaceans and aquatic plants. Farming implies some intervention in the rearing process to enhance production, such as regular stocking, feeding and protection from predators. Artificial feeding of fish is one of the principal ways of increasing production in fish farming. In intensive fish farming artificial feeding is essential for growth and even in extensive farming, some artificial feeding is usually required. The majority of fish farmed in intensive aquaculture systems in the EU are carnivorous, having a high requirement for protein in their diets. Generally, fishmeal is used as the major source of protein in feeds formulated for cold-water fish rations. Because many species of fish, which are farmed, are carnivorous by nature they feed on other species of fish and crustaceans. Consequently, the feed of farmed marine and freshwater fish is mainly composed of re-cycled dead fish in the form of fishmeal and fish oil. The fishmeal is predominantly produced from a variety of ocean-caught marine fish. Farmed and wild fish also often have particular dietary requirements in relation to fats and amino acid requirements. The salmonids have a requirement for omega-3 (n-3) fatty acids of longer chain lengths and certain amino acids.
Consequently, the most important ingredient in the diets of farmed fish is fishmeal. Mammalian-derived materials have also been used, to some extent, as an ingredient for feeding farmed marine and freshwater fish. For example, up to recently, blood meal was used in fish feeds. However, because of EU legislation banning such ingredients, it is no longer used. Fishmeal is obtained from whole dead wild caught fish or trimmings of such fish after filleting for human consumption The most widely used technique for fish meal processing is the wet reduction process, which is operated continuously and requires large amounts of raw material. The fish is steam cooked and pressed. The pressing of the cooked fish results in a protein fraction called press cake, and a mixed water and oil fraction with suspended and soluble protein. Oil and the water fraction with proteins are separated. The stick water is concentrated through evaporation. The temperature used, particularly at the drying stage, should be hot enough to kill any bacteria but not so hot that it denatures the protein. A drying temperature of 15-80°C is usually considered optimum. The feeding with fishmeal raises the question of intra-species or intra-order recycling of fish tissues. Generally, although recycled fish in the form of fishmeal is the principle ingredient of food for farmed fish, recycled farmed fish tissues are not used as an ingredient of fishmeal produced for fish feeds. Even if intra-species recycling of fish tissue did occur, the heat and drying treatment used to produce fishmeal should be sufficient to destroy any conventional fish or human pathogens, but not TSE agents if present.
4. RESEARCH ON TSEs IN FISH
4.1. THE EC FAIR CT97 3308 PROJECT: “SEPARATION, IDENTIFICATION AND CHARACTERISATION OF THE NORMAL AND ABNORMAL ISOFORMS OF PRION PROTEIN FROM NORMAL AND EXPERIMENTALLY INFECTED FISH” The project, has four principle objectives with corresponding results summarized as follows:
1: Characterization of normal isoforms of fish PrP and its coding nucleotide sequence: The amphibian (X. Laevis) PrP was sequenced. Using probes designed for screening fish cDNA, some clones showed homology with the prion probe and were partially sequenced, but it is unclear from these data if a true PrP sequence was identified. A final conclusion will be drawn after complete sequence data of all the clones.
2: Attempted transmission of TSE to fish from ovines and bovines: several different species of fish were inoculated with scrapie and BSE infected material. Trout and turbot were inoculated simultaneously (intracerebrally, intra-peritoneally and intramuscularly) with scrapie infected material and trout and sea bream were inoculated with BSE infected material. Scrapie agent inoculated turbot had infectivity as demonstrated by mouse inoculation in brain and spleen (15 days post inoculation [pi]) and brain (90 days pi). Infectivity was also found to persist sporadically in the intestine of fish fed with high doses of scrapie infected material. Trout and sea bream which were inoculated with BSE material did not show evidence of infection up to four months pi. The transmission experiments with tissues from fish infected with scrapie are still in progress. Otherwise the experiments with material from fish infected with BSE are completed. (Further detail of the outcome of the transmission studies is given in APPENDIX)
3: Establishing a diagnostic test for PrP detection in fish tissues. As this is dependent on the outcome of objective 1, no test has yet been developed.
4: Evaluation of the uptake and binding of normal fish PrP. It was not possible to draw conclusions.
Comment on experimental studies:
a) The transmission protocol maximises the chance of identifying residual inoculum and minimises the chances of identifying agent, which has infected the fish and is being amplified/replicated in the fish tissue because:
The inoculum used is mouse adapted scrapie (139A)
Mouse (unspecified strain/panel) bioassay is being used for detection of infectivity in fish tissues
There is no evidence that any of the antibodies use on fish tissues for IHC or WB have any cross reactivity with “fish PrP”.
There has been no sub-passage of tissues from exposed fish in fish of the same species. This would be the only practical way of addressing the question of whether fish can be infected, the problems of adaptation through intra-specific passage etc.
b) The research project has, so far, not found any evidence for replication of TSE agents in fish. This is in line with negative results of searches in fish databases, which were unable to detect a sequence with similarities to known prions (Joly et al., 2001), from which it was concluded that a potential fish PrP gene is probably very different from those characterised in mammals and that it would be extremely unlikely to share common pathological properties.
However, this is somewhat in contradiction with the data from Gibbs et al (1997) describing, for the first time, the presence of a normal isoform of amyloid protein (PrP) in brains of spawning salmon. Also, in contrast is a recent publication (Suzuki et al., 2002) identifying a PrP-like molecule in the pufferfish (Fugu rubripes), showing high homology with mammalian PrP sequences, but some structural inconsistency. These are the only available data at present, clearly demonstrating that a lot more needs to be known about piscine PrP genes, PrP and variation in sequences of each.
c) The final outcome of the project should contribute to the understanding as to whether fish are possible carriers of residual infectivity or whether there is direct evidence of transmission of TSE to fish. it should also inform on the potential risk connected to fish derived foods for human and animal, the establishment of analytical protocols for PrP detection in fresh fish food and the comparison of the molecular properties of normal and abnormal isoforms of PrP.
4.2. OTHER DATA ON TSES IN FISH
The availability of (recent) data and research results on TSEs in fish is quite limited. In its report2 in support of its opinion of 24-25 June 1999 on “Fallen stock”, the SSC concluded as follows: “So far, no evidence for TSE in fish was found. Alderman (1996) reports that the Fish Diseases laboratory at Weymouth (UK) has for 25 years been involved in studying the diseases of marine and freshwater fish. During that time the laboratory has not observed any scientific evidence of any condition which might in any way be described as a spongiform encephalopathy in fish, whether of species used to produce fishmeal, or directly for human food, from the UK, other EU member states or from elsewhere in the world. What precedes is confirmed by Professor Hugh Ferguson of the Institute of Aquaculture at Stirling University (SEAC, 1999, communication to the SSC secretariat).
He reports that fish brains are examined quite frequently, and in young fish often as a result of investigations for gill infections. As there are recognized diseases of fish that could cause vacuolation, fish experts are conscious of concerns about TSEs. Nothing suggestive of a TSE has been found however.” The TSE/BSE ad hoc Group considers that both from the literature and from limited observations on fish, there is no evidence that TSEs would naturally exist in fish but 2 Scientific Report on The risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials.
Adopted By the Scientific Steering Committee at its meeting of 24-25 June 1999.
that the possibility cannot be totally excluded. More research is required to improve the confidence of this conclusion.
5. THE RISK OF RECYCLING OF FISH WITH REGARD TO TSES
5.1. GENERAL
The epidemiological risk depends on the origin and properties of the raw material and the field of application of the product. Unfortunately, from an economic point of view, recycling as feed is the most profitable way, but also theoretically the most dangerous way, of dealing with animal by-products. Intra-species recycling could be regarded as more dangerous than producing feed for phylogenetically less related species, because of possible species barrier effects. However, in the absence of any data on species barrier effect in fish, the potential importance of intra-species recycling versus intra-order recycling cannot be estimated at present and neither are indications available that recycling in fish can be considered in the same context as is done for the domestic animal situation. In this respect reference can be made to the natural and experimental transmission history of mammalian TSE’s, suggesting a wide phylogenetic susceptibility within the Order. In the cases of BSE and CWD the species barrier, in terms of oral route, is probably negligible across several species of the respective phylogenetic families and subfamilies of the host. The kudu may be even more susceptible for BSE than domestic cattle and BSE also affects Felidae under “recycling” conditions. Nevertheless, as long as the TSE problem is not relevant for fish and meat and bone meal from other possibly TSE infected species is not used as feed in aquaculture, recycling would not create an increased risk in respect to TSE in fish. The assessment would have to be reviewed, in line with the general principles of intra-species or intraorder recycling, if evidence is found of replication of TSE agent in fish. The use of resulting products as fertiliser further reduces the epidemiological risk of recycling of organic wastes with respect to direct transmission to susceptible hosts but it increases the risk of uncontrolled and indirect transmission to susceptible hosts or exposed materials with epidemiological importance as feed or food. In addition, if TSE was to be shown to exist in fish, the process designed for treatment of fish material in order to produce a fertiliser must be designed in such a way that the TSE agent is maximally inactivated. The safest way for treating organic wastes of animal origin is processing at 133 °C under 3 bar steam pressure for at least 20 min. If this causes technological problems which might be expected with fish material other time/temperature relationships may be applied but they have to be validated. Fishmeal is obtained from drying, heating and pressing of whole dead wild caught fish or trimmings of such fish after filleting for human consumption. Generally, although recycled fish tissues in the form of fishmeal is the principle ingredient of food for farmed fish, recycled farmed fish are not used as an ingredient of fishmeal produced for fish feeds. Even if intra-species recycling of fish did occur, the heat and drying treatment used to produce fishmeal should be sufficient to destroy any conventional fish or human pathogens, but not totally TSE agent.
5.2. THE POSSIBILITIES OF TSE’S BEING RECYCLED IN FISH.
Wild fish Many species of wild fish are carnivorous. There are two main scenarios that may result in a build-up of TSE’s in wild fish. Firstly, it is possible to hypothesise that a spontaneous TSE could develop in wild fish and that wild sea or river fish would have the capacity to recycle a TSE. In wild sea fish any pelagic fish (which move continuously in shoals and are the major source of fishmeal for farmed fish) a TSE might conceivably manifest in the early stages as an inability to swim properly, the individual fish would fall out of the shoal and become the prey of larger members of its own or other species eg demersal (ground level, solo feeders) or marine mammals. Such fish or mammals could then become "infected" and eventually fall prey to further carnivorous fish of the same or other species or marine mammals. A mature or semi-mature “infected” fish would most likely be eaten by a larger member of its own or another species. If the biological principles of infection with TSE in fish is similar to that in mammals, it may be difficult for adult fish to become infected by eating “infected” material. However, even in mammals, little is known about age related differences of susceptibility to TSE, but it is possible, as suspected for BSE in cattle that, also in fish, adults are less susceptible than the young of the species.
In the absence of information on the ID50 and mean incubation times for TSE’s in any sea or freshwater fin fish only assumptions may be made. It is likely that natural predation would offer limited scope for amplification of the agent and the “infectivity" could remain confined to a small number of the sea or freshwater fish or mammals.
The second scenario involves direct exposure to TSE infected mammalian carcasses or their parts. Pelagic, demersal sea fish or freshwater fish could be directly exposed to mammalian TSE’s through direct exposure to a dead TSE infected animal or its parts. Such an exposure could, as with the case of a spontaneous development of a fish TSE, initiate a cycle which could be propagated to other pelagic, demersal, freshwater (coarse or game) fish or marine of freshwater mammals. However, as for spontaneous development and under natural predation conditions, it is unlikely that significant amplification would occur among wild fish. Dumping fish waste/offal at sea or in fresh water is likely to increase any theoretical possibility of recycling a TSE among wild fish as all ages, and sizes of fish could consume the waste.
Farmed fish
Farmed fish in general, need a protein source in their feed that originates from fish and is generally provided by a diet based on fishmeal. For this reason the possibility of recycling a TSE in farmed fish would be greater than is the case for wild fish. To date, there is no evidence of a TSE in wild fish and therefore, no obvious possibility of “infected” wild fish being caught and processed into fishmeal. Likewise, although scavengers such as crustaceans or even marine mammals could also be infected, such fish or animals generally have a limited contribution to fishmeal. However, even a low-grade infection in the source fish could initiate a cycle in farmed fish if entire, or parts of, “infected” farmed fish were recycled without measures being taken to inactivate TSE’s. It is possible that without treatment to inactivate infectious prions, fishmeal and fish oil could transmit “infectious” prions to farmed fish. The processing parameters for fishmeal (generally a temperature of 85°C is used with other physical processes) would not inactivate infectious prions. If materials from farmed fish were processed at these parameters only, and then fed back to farmed fish recycling of infectious prions to fish or to mammals could occur. Intra-species recycling, due to the absence of a species barrier could increase the risk that TSE cases occur or undetected pools of infectivity develop. However, although intra-species recycling could be regarded as more dangerous than producing feed for phylogenetically less related species, because of possible species barrier effects, in the absence of any data on species barrier effect in fish, the potential importance of intra-species recycling versus intra-order recycling cannot be estimated at present and neither are indications available that recycling in fish can be considered in the same context as is done for the domestic animal situation.
Farmed fish in Europe could have been exposed to feed containing meal derived from the blood of ruminants. However blood from ruminants is considered to be low risk by the oral route for transmission of ruminant TSE’s, when taking into account the recommendations in the SSC opinion of 13-14 April 2000 on the “Safety of ruminant blood with respect to TSE risks” Farmed fish could likewise be directly exposed to a mammalian TSE by direct exposure to an infected dead animal or its parts. This is an unlikely, but possible scenario. Recycling farmed fish as feed for other farmed fish would greatly increase the risk of amplifying a TSE in fish and should be avoided.
5.3. SSC OPINIONS ON THE RISK OF RECYCLING OF FISH WITH REGARD TO TSE
From chapters 3 and 4, it can be concluded that to date there has been no evidence of TSE found in fish. Fish brain is examined quite routinely in fish disease diagnosis and to date no changes similar to those described for TSE have been reported. However, it should be taken into account that a prion infection in fish might not present as an obvious TSE. In addition, the above mentioned FAIR CT97 3308 research project is looking at normal and abnormal prion proteins in fish and has, so far, not found any evidence for replication of TSE in fish3. However, the possibility cannot be totally excluded as in a recent publication (Suzuki et al., 2002) a homologue to prion-protein was identified in the pufferfish Fugu rubripes, showing high homology with mammalian PrP sequences and Gibbs et al (1997) described for the first time the presence of normal isoform of amyloid protein (PrP) in brains of spawning salmon. These are the only available data at present, clearly demonstrating that a lot more needs to be known about piscine PrP genes, PrP and variation in sequences of each. 3 The final outcome of that project should contribute to the assessment of the possibility of transmission of TSE to fish, the evaluation of the potential risk connected to fish derived foods for human and animal, the establishment of analytical protocols for PrP detection in fresh fish food and the comparison of the molecular properties of normal and abnormal isoforms of PrP.
Intra-species or intra-order recycling of fish should not present a risk with regard to TSEs, provided a number of conditions are satisfied. These conditions have already been listed in various SSC opinions and reports. The TSE/BSE ad hoc Group considers that they are still valid.
The opinions of interest can be listed as follows:
a. The opinion on “The risk born by recycling animal by-products as feed with regard to propagating TSE in non-ruminant farmed animals”, adopted on 17 September 1999. In general, this opinion recognises the recycling of animal by-products processed into basic biochemical substances as fat and protein this as an acceptable effective way of re-use of valuable materials. It accepts that intra-species recycling can be acceptable when the material of origin is from epidemiological point of view safely sourced with regard to TSE's and treated accordingly to prevent any spread of conventional diseases. It also notes that current disease monitoring systems are regarded to be unlikely to identify sporadic cases of TSE’s in farmed fish. Monitoring of pathological changes wild fish over a period of 25 years for neurological disorders, on the other hand, has provided no anecdotal evidence leading to any indications of spongiform encephalopathies in fish.
b. The SSC opinion of 24-25 June 1999 on “Fallen stock”4, which clarifies what can be considered as safe sourcing of fish materials and the processing conditions to be applied to fish waste.
c. Opinion of the Scientific Steering Committee (1) on the scientific basis for import bans proposed by 3 Member States with regard to BSE risks in France and the Republic of Ireland;
(2) on the scientific basis for several measures proposed by France with regard to BSE risks;
(3) and on the scientific basis for banning animal protein from the feed for all farmed animals, including pig, poultry, fish and pet animals.
Adopted by the Scientific Steering Committee at its meeting of 27-28 November 2000 This opinion provides the possible scientific reasons for a general feed ban of meat-and-bone meal, applicable to all farmed animals including cattle, pigs, poultry, farmed fish and pet food.
6. REFERENCES
EC (European Commission) (1999a). Scientific Opinion of the Scientific Steering Committee on the risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials. Adopted by the Scientific Steering Committee at its meeting of 24-25 June 1999 4 Scientific Opinion on The risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials. Adopted By the Scientific Steering Committee at its meeting of 24-25 June 1999.
F:\WebDev\TSE in fish_OPINION_0303_FINAL.doc 12
EC (European Commission) (1999b). Scientific Opinion of the Scientific Steering Committee on The risk born by recycling animal by-products as feed with regard to propagating TSE in non-ruminant farmed animals. Adopted by the Scientific Steering Committee at its meeting of 17 September 1999 EC (European Commission) (2000). Scientific Steering Committee Opinion on the Scientific basis for import bans proposed by 3 member states with regard to BSE risks in France and the Republic of Ireland; on the Scientific basis for several measures proposed by France with regard to BSE risks and on the Scientific basis for banning animal protein from feed for all farmed animals, including pig, poultry, fish and pet animals. Adopted by the Scientific Steering Committee at its meeting of 27-28 November 2000 EC (European Commission) (2002). Interim results (2002) of the FAIR CT97 3308 project entitled “Separation, identification and characterisation of the normal and abnormal isoforms of prion protein from normal and experimentally infected fish” EC (European Commission) (2002). Scientific Committee on Animal Health and Animal Welfare (2002). Draft report on “The use of fish waste in aquaculture.” Gibbs, C.J., Bolis, C.L., 1997. Normal isoform of amyloid protein (PrP) in brains of spawning salmon. Molecular Psychiatry, 2, 146-147. Joly, J.S., Nguyen V., Bourrat F., 2001. Conservation of the prion proteins in Vertebrates. (Conservation des "prions" chez les Vertebres.). Productions-Animales (Paris), Mai, 2001, Vol. 14, No. 2, P. 91-96, Print Issn: 0990-0632. Schoon, H.A., Brunkhorst, B., Pohlenz, J., 1991. Beitrag zur neuropthologie beim Rothalsstrauss (Struthio camelus) - Spongiforme Enzephalopathie. Vehr.ber Erkrg. Zootiere 33, Acad Verl. 309-313. Schoon, H.A., Brunkhorst, B., Pohlenz, J., 1991. Spongiforme Enzephalopathie beim Rothalsstrauss (Struthio camelus). Tierarztl Prax, 19, 263-265 Suzuki T., Kurokawa T., Hashimoto H., Sugiyama M., 2002. cDNA sequence and tissue expression of Fugu rubripes prion protein-like: a candidate for the teleost orthologue of tetrapod PrPs. BBRC, 294, 912-
F:\WebDev\TSE in fish_OPINION_0303_FINAL.doc 13
APPENDIX: THE EC FAIR CT97 3308 PROJECT:
“Separation, identification and characterisation of the normal and abnormal isoforms of prion protein from normal and experimentally infected fish” Studies of the transmissibility of scrapie to fish
a. Experimental transmission:
Groups of 30 Trout (Onchorrhychus mykiss) and Turbot (Scophtalmus maximus) were inoculated with mouse adapted scrapie agent (strain 139A) by simultaneous intracerebral (i.c.), intra peritoneal (i.p.) and intra muscular (i.m.) routes. There were 15 control animals per group.
Brain, spleen, muscle, liver, intestine, kidney from 3 infected and one control fish were sampled at each of the following time points:.
15 days post inoculation (pi), 3 months pi, 6 months pi and every 6 months thereafter.
All tissues were inoculated into mice and fixed for immunohistochemical studies. The incomplete results are summarised in the following table, showing the number of mice positive/ number of mice inoculated (unconfirmed/pending result) Postinoculation Turbot Trout Brain Spleen brain Spleen 15 days 2/8 (1) 4/7 (0) 90 days 1/8 (7) 0/8 (5) 180 days - - 360 days - - Every 6 months thereafter No results yet available, all mice still alive No lesions were detected so far in infected fish tissues, IHC is being performed on those tissues which were positive on assay in mice.
b. Assessment of residual infectivity:
Turbot and Trout force fed 139A scrapie infected or normal mouse brain homogenate and samples taken of brain, intestine, muscle at 1, 15, 30, 60 and 90 days.
Residual infectivity was detected on mouse bioassay only in one of eight mice, which had been inoculated with Trout intestine, taken 1 day after oral inoculation. Results from scrapie transmissions to mice from fish more than 90 days post inoculation are awaited.
Infectivity also found to persist sporadically in intestine of fish fed with high doses of scrapie.
F:\WebDev\TSE in fish_OPINION_0303_FINAL.doc 14
Studies of the transmissibility of BSE to fish :
Experimental Transmission
Groups of Trout and Sea Bream (Spaurus aurata L.) were fed or were inoculated i.c with BSE affected bovine material. Approx. 40 experimental and 15 control in each group.
Abnormally swimming animals sacrificed and brains dissected. Samples (brain, muscle, spleen, liver, intestine, reproductive organs, eye, kidney) taken 1, 2, 15, 30, 60, 90, 120 days pi.
No abnormal swimming between 1 to 120 days. No evidence of infection by histology, IHC or Western blot (prionics). Histological findings: No evidence of significant changes in the brains or other organs studied from fish sampled at 1, 2, 15, 30, 60, 90 and 120 days pi.
Immunohistochemical findings: by using ABC-peroxidase technique with mAbs 2A11 and 6H4, no evidence of PrPres deposition has been detected in any sample. The effectiveness of McAb 2A11 on bovine and murine prion infected brains was previously verified with ABC-peroxidase technique, and immunohistochemistry with 6H4 was performed as described previously. However, in the absence of positive TSE infected fish controls and the uncertainty of the existence of a molecule in fish equivalent to mammalian PrP, the efficacy of these antibodies for detection of any surrogate marker for TSE infectivity in fish is unknown.
Western blot technique: by using the “Prionics test” (mAb 6H4), every sample of all the groups were negative to the presence of proteinase-K resistant prion protein.
It must be remembered that the present period of observation (4 months) is probably not sufficient to provide evidence that would make distinction between residual inoculum infectivity and pathogenetic amplification of agent. In a further experimental step the project proposes to evaluate the possible transmission of prions (Scrapie and BSE) to different fish species (Sea Bream, Sea Bass (Dicentrarchus labrax L.) and Trout). The ultimate test would be to feed back/inoculate material from fish experimentally challenged into more fish of the same species. This should be considered.
http://europa.eu.int/comm/food/fs/sc/ssc/out320_en.pdf
3.4. Conclusions
The SSC, in considering the possible consequences, concludes as follows:
A. So far no scientific evidence exists to demonstrate the natural occurrence of TSE in farmed pigs, poultry and fish, which may create a basis for an intra-species progression of a TSE infection due to intra-species recycling.
B. Given the limitations of the surveillance in certain areas, and the length of the incubation time in relation to the normal (=economic or commercial) life span of the animals, it can not be excluded that cases occur and that, perhaps more important, an undetected pool of infectivity is build up.
C. Because of these two preceding points, the SSC wants to underline that in scientific terms absence of evidence is neitherevidence of absence nor of presence of a risk. However, it is impossible to exclude, on the basis of the available evidence, that TSEs are already present (albeit undetected) in non-ruminant farmed animals, in particular not if there is reason to assume that these species have been (and might still be) exposed to BSE-contaminated feed (produced from ruminants).
D. Recycling of animal material, in general, will increase the risk that cases occur or undetected infectivity pools develop,in particular if potentially BSE (TSE) contaminated material is recycled to ruminants or (possibly) susceptible non-ruminants.
E. Intra-species recycling will, due to the absence of a species barrier, increase the risk further.
F. If recycling, and in particular intra-species recycling, of animal material to farmed animals can not be avoided, all measures that reduce the recycled infectivity would reduce the risk.
G. Measures that reduce the recycled infectivity include 6 :
- exposing the recycled animal material to a treatment by 133°/20'/3b or equivalent conditions,
- excluding those tissues known to carry the highest infectious load (SRM 7 ),
- excluding 8 fallen stock from the production of feed,
- stop feeding pig, poultry or fish potentially contaminated feed a sufficiently long period of time before slaughter in order to reduce the risk of recycling infectivity via the gut-content.
H. It has to be understood that
- the possible measures would not be able to reach a zero risk should infectivity enter the recycling loop, and
- that due to the long incubation time of this type of disease a significant risk would have build up before an incidence becomes visible (as has been seen in the case of BSE in the UK).
I. The SSC considers R&D in the field of surveillance and (pre-clinical) diagnostic of TSEs and the experimental transmission of TSEs to farmed (non-ruminant) animals to be of highest priority.
http://ec.europa.eu/food/fs/sc/ssc/out60_en.html
OPINION ON : THE FEEDING OF WILD FISHMEAL TO FARMED FISH AND RECYCLING OF FISH WITH REGARD TO THE RISK OF TSE ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 6-7 MARCH 2003.
http://ec.europa.eu/food/fs/sc/ssc/out320_en.pdf
APPENDIX: THE EC FAIR CT97 3308 PROJECT:
“Separation, identification and characterisation of the normal and abnormal isoforms of prion protein from normal and experimentally infected fish”
Studies of the transmissibility of scrapie to fish
a. Experimental transmission:
Groups of 30 Trout (Onchorrhychus mykiss) and Turbot (Scophtalmus maximus) were inoculated with mouse adapted scrapie agent (strain 139A) by simultaneous intracerebral (i.c.), intra peritoneal (i.p.) and intra muscular (i.m.) routes. There were 15 control animals per group.
Brain, spleen, muscle, liver, intestine, kidney from 3 infected and one control fish were sampled at each of the following time points:. 15 days post inoculation (pi), 3 months pi, 6 months pi and every 6 months thereafter.
All tissues were inoculated into mice and fixed for immunohistochemical studies. The incomplete results are summarised in the following table, showing the number of mice positive/ number of mice inoculated (unconfirmed/pending result)
Postinoculation
Turbot Trout
Brain Spleen brain Spleen
15 days 2/8 (1) 4/7 (0)
90 days 1/8 (7) 0/8 (5)
180 days - -
360 days - -
Every 6 months thereafter No results yet available, all mice still alive
No lesions were detected so far in infected fish tissues, IHC is being performed on those tissues which were positive on assay in mice.
b. Assessment of residual infectivity:
Turbot and Trout force fed 139A scrapie infected or normal mouse brain homogenate and samples taken of brain, intestine, muscle at 1, 15, 30, 60 and 90 days.
Residual infectivity was detected on mouse bioassay only in one of eight mice, which had been inoculated with Trout intestine, taken 1 day after oral inoculation. Results from scrapie transmissions to mice from fish more than 90 days post inoculation are awaited.
Infectivity also found to persist sporadically in intestine of fish fed with high doses of scrapie.
F:\WebDev\TSE in fish_OPINION_0303_FINAL.doc 14
Studies of the transmissibility of BSE to fish :
Experimental Transmission
Groups of Trout and Sea Bream (Spaurus aurata L.) were fed or were inoculated i.c with BSE affected bovine material. Approx. 40 experimental and 15 control in each group.
Abnormally swimming animals sacrificed and brains dissected. Samples (brain, muscle, spleen, liver, intestine, reproductive organs, eye, kidney) taken 1, 2, 15, 30, 60, 90, 120 days pi.
No abnormal swimming between 1 to 120 days. No evidence of infection by histology, IHC or Western blot (prionics).
Histological findings: No evidence of significant changes in the brains or other organs studied from fish sampled at 1, 2, 15, 30, 60, 90 and 120 days pi.
Immunohistochemical findings: by using ABC-peroxidase technique with mAbs 2A11 and 6H4, no evidence of PrPres deposition has been detected in any sample. The effectiveness of McAb 2A11 on bovine and murine prion infected brains was previously verified with ABC-peroxidase technique, and immunohistochemistry with 6H4 was performed as described previously. However, in the absence of positive TSE infected fish controls and the uncertainty of the existence of a molecule in fish equivalent to mammalian PrP, the efficacy of these antibodies for detection of any surrogate marker for TSE infectivity in fish is unknown.
Western blot technique: by using the “Prionics test” (mAb 6H4), every sample of all the groups were negative to the presence of proteinase-K resistant prion protein.
It must be remembered that the present period of observation (4 months) is probably not sufficient to provide evidence that would make distinction between residual inoculum infectivity and pathogenetic amplification of agent.
In a further experimental step the project proposes to evaluate the possible transmission of prions (Scrapie and BSE) to different fish species (Sea Bream, Sea Bass (Dicentrarchus labrax L.) and Trout). The ultimate test would be to feed back/inoculate material from fish experimentally challenged into more fish of the same species. This should be considered.
http://ec.europa.eu/food/fs/sc/ssc/out320_en.pdf
Conclusions:
The unique characteristics of prions will offer many new avenues for research. There is compelling evidence of the role of prions in TSE diseases, but the cause - effect relationship in animals remains a hypothesis. Research shows that PrP’s can persist in intestinal and caeca submucosa of fishes (Chiesa & Harris 2009) following oral administration. However, the hypothesis in mammals that misfolded prions are multiplied in the intestine and then exported is not the same in fish, as the fish intestine produces a very small amount of prions and the wrong kind. The theory that fish fed MBM though either natural feeding or manufactured feeds play a role in the transmission of TSE’s is far from a scientific validated statement. To suggest additional regulation is needed “just in case,” because “we don’t know for sure” would be irresponsible.
http://assets.nationalrenderers.org/Fish_and_Prions.pdf
Scrapie infectivity is quickly cleared in tissues of orally-infected farmed fish
Loredana Ingrosso1 , Beatriz Novoa2 , Andrea Z Dalla Valle3 , Franco Cardone1 , Raquel Aranguren2 , Marco Sbriccoli1 , Simona Bevivino1 , Marcello Iriti4 , Quanguo Liu1 , Vito Vetrugno1 , Mei Lu1 , Franco Faoro4 , Salvatore Ciappellano3 , Antonio Figueras2 and Maurizio Pocchiari1
1 Istituto Superiore di Sanità, Department of Cellular Biology and Neuroscience, viale Regina Elena,299,00161 Rome, Italy
2 Instituto Investigaciones Marinas, CSIC, Eduardo Cabello 6, 36208 Vigo, Spain
3 Section of Human Nutrition, Department of Food Science and Microbiology, DiSTAM, University of Milan, via Celoria 2, 20133 Milano, Italy
4 Institute of Plant Pathology, University of Milan and Institute of Plant Virology, CNR, Milano, Italy
author email corresponding author email
BMC Veterinary Research 2006, 2:21doi:10.1186/1746-6148-2-21
The electronic version of this article is the complete one and can be found online at:
http://www.biomedcentral.com/1746-6148/2/21
Received: 28 March 2006 Accepted: 15 June 2006 Published: 15 June 2006
© 2006 Ingrosso et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background
Scrapie and bovine spongiform encephalopathy (BSE) belongs to the group of animal transmissible spongiform encephalopathy (TSE). BSE epidemic in the UK and elsewhere in Europe has been linked to the use of bovine meat and bone meals (MBM) in the feeding of cattle. There is concern that pigs, poultry and fish bred for human consumption and fed with infected MBM would eventually develop BSE or carry residual infectivity without disease. Although there has been no evidence of infection in these species, experimental data on the susceptibility to the BSE agent of farm animals other than sheep and cow are limited only to pigs and domestic chicken. In the framework of a EU-granted project we have challenged two species of fish largely used in human food consumption, rainbow trout (Oncorhynchus mykiss) and turbot (Scophthalmus maximus), with a mouse-adapted TSE strain (scrapie 139A), to assess the risk related to oral consumption of TSE contaminated food. In trout, we also checked the "in vitro" ability of the pathological isoform of the mouse prion protein (PrPSc) to cross the intestinal epithelium when added to the mucosal side of everted intestine.
Results
Fish challenged with a large amount of scrapie mouse brain homogenate by either oral or parenteral routes, showed the ability to clear the majority of infectivity load. None of the fish tissues taken at different time points after oral or parenteral inoculation was able to provoke scrapie disease after intracerebral inoculation in recipient mice. However, a few recipient mice were positive for PrPSc and spongiform lesions in the brain. We also showed a specific binding of PrPSc to the mucosal side of fish intestine in the absence of an active uptake of the prion protein through the intestinal wall.
Conclusion
These results indicate that scrapie 139A, and possibly BSE, is quickly removed from fish tissues despite evidence of a prion like protein in fish and of a specific binding of PrPSc to the mucosal side of fish intestine.
http://www.biomedcentral.com/1746-6148/2/21
Research paper
Generation and characterisation of monoclonal antibodies to Rainbow trout (Oncorhynchus mykiss) prion protein
References and further reading may be available for this article. To view references and further reading you must purchase this article.
B.C. Maddisona, S. Patela, R.F. Jamesb, H.E. Conlonc, B. Oidtmannd, e, M. Baierf, G.C. Whitelamc and K.C. Gougha, ,
aADAS, Animal Health and Welfare, Biotechnology Group, Department of Biology, University of Leicester, Adrian Building, University Road, Leicester, LE1 7RH, Leicestershire, UK
bDepartment of Infection, Immunity and Inflammation, University of Leicester, University Road, Leicester, LE1 9HN, UK
cDepartment of Biology, University of Leicester, University Road, Leicester, LE1 7RH, UK
dCEFAS, Weymouth Laboratory, The Nothe, Weymouth, Dorset DT4 8UB, UK
eInstitute of Zoology, Fish Biology and Fish Diseases, University of Munich, 80539 Munich, Germany
fNeurodegenerative Diseases, Robert-Koch-Institut, Nordufer 20, 13353 Berlin, Germany
Received 17 May 2005; revised 26 July 2005; accepted 7 September 2005. Available online 27 September 2005.
Abstract
We report the production and characterisation of three monoclonal antibodies to the prion protein (PrP) of Rainbow trout (Oncorhynchus mykiss), a piscine protein with characteristic structural features common to mammalian prion protein. All of the antibodies were used to detect PrP in ELISA, Western blot and by immunohistochemistry. The antibodies showed specificity for certain genera of the Salmonidae, binding to PrP of Rainbow trout and Atlantic salmon (Salmo salar) but not to that from Arctic char (Salvelinus alpinus). Using the immunoreagents in Western blots, we demonstrated that O. mykiss PrP protein is a 64 kDa protein present in brain, spinal chord and optic nerve. PrP was not detected in a range of peripheral tissues: eye, heart, stomach, intestine, liver, kidney, spleen, muscle and skin. Furthermore, PrP could be detected in all brain regions studied: optic lobe, cerebrum/olfactory lobe, cerebellum, hypothalamus/pituitary and medulla oblongata and was widespread within these tissues as determined by immunohistochemistry. These immunoreagents provide specific tools to study the biology of Rainbow trout and Atlantic salmon PrP and any possible transmissible spongiform encephalopathy-like disease of these economically important fish species.
Keywords: Prion protein; Fish; Salmonidae; PrP; Antibodies
Abbreviations: PrP, prion protein; TSE, transmissible spongiform encephalopathy; AP, alkaline phosphatase; pNPP, para-nitrophenyl phosphate; CNS, central nervous system; TBS, tris-buffered saline; HRP, horse-radish peroxidase; IMS, Industrial Methylated Spirits; BCIP/NBT, 5-bromo-4-chloro-3-indolylphosphate/nitroblue tetrazolium; LB, Luria-Bertani media
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T2Y-4H6GW7D-2&_user=10&_coverDate=11%2F30%2F2005&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=68d737722d1a1f1d56c841d715eb2fff&searchtype=a
Evaluation of the Possible Transmission of BSE and Scrapie to Gilthead Sea Bream (Sparus aurata)
Evgenia Salta1#, Cynthia Panagiotidis2#, Konstantinos Teliousis3, Spyros Petrakis1,4, Eleftherios Eleftheriadis5, Fotis Arapoglou5, Nikolaos Grigoriadis6, Anna Nicolaou7, Eleni Kaldrymidou3, Grigorios Krey5, Theodoros Sklaviadis2*
1 Department of Pharmacology, Aristotle University of Thessaloniki, Thessaloniki, Greece, 2 Centre for Research and Technology-Hellas, Institute of Agrobiotechnology, Thessaloniki, Greece, 3 Laboratory of Pathology, School of Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece, 4 Max Delbruck Center for Molecular Medicine, Department of Neuroproteomics, Berlin-Buch, Germany, 5 National Agricultural Research Foundation, Fisheries Research Institute, Nea Peramos, Greece, 6 B' Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece, 7 Department of Business Administration, University of Macedonia, Thessaloniki, Greece
In transmissible spongiform encephalopathies (TSEs), a group of fatal neurodegenerative disorders affecting many species, the key event in disease pathogenesis is the accumulation of an abnormal conformational isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). While the precise mechanism of the PrPC to PrPSc conversion is not understood, it is clear that host PrPC expression is a prerequisite for effective infectious prion propagation. Although there have been many studies on TSEs in mammalian species, little is known about TSE pathogenesis in fish. Here we show that while gilthead sea bream (Sparus aurata) orally challenged with brain homogenates prepared either from a BSE infected cow or from scrapie infected sheep developed no clinical prion disease, the brains of TSE-fed fish sampled two years after challenge did show signs of neurodegeneration and accumulation of deposits that reacted positively with antibodies raised against sea bream PrP. The control groups, fed with brains from uninfected animals, showed no such signs. Remarkably, the deposits developed much more rapidly and extensively in fish inoculated with BSE-infected material than in the ones challenged with the scrapie-infected brain homogenate, with numerous deposits being proteinase K-resistant. These plaque-like aggregates exhibited congophilia and birefringence in polarized light, consistent with an amyloid-like component. The neurodegeneration and abnormal deposition in the brains of fish challenged with prion, especially BSE, raises concerns about the potential risk to public health. As fish aquaculture is an economically important industry providing high protein nutrition for humans and other mammalian species, the prospect of farmed fish being contaminated with infectious mammalian PrPSc, or of a prion disease developing in farmed fish is alarming and requires further evaluation.
Citation: Salta E, Panagiotidis C, Teliousis K, Petrakis S, Eleftheriadis E, et al. (2009) Evaluation of the Possible Transmission of BSE and Scrapie to Gilthead Sea Bream (Sparus aurata). PLoS ONE 4(7): e6175. doi:10.1371/journal.pone.0006175
Editor: Etienne Joly, Université de Toulouse, France
Received: March 27, 2009; Accepted: May 19, 2009; Published: July 28, 2009
Copyright: © 2009 Salta et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was funded by the European Commission's Food Quality and Safety: Prevention, Control, Treatment, Management and Risk analysis of Prion Diseases, Neuroprion (NOE), Grant ID: FOOD-CT-2004-506579, URL: http://www.neuroprion.org/en/np-neuropri?on.html and TSE & Fish: Evaluation of the possible transmission of prions (Scrapie and BSE) to different fish species, Grant ID: QLK5-2002-00866, URL:
http://ec.europa.eu/research/agriculture?/projects/qlrt_2001_00866_en.htm
Evgenia Salta is a scholar of the Greek States Scholarships Foundation,
URL: http://www.iky.gr/.
The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
* E-mail: sklaviad@auth.gr
# These authors contributed equally to this work.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0006175
Prion. 2009 Jul–Sep; 3(3): 129–133. PMCID: PMC2802776
Copyright © 2009 Landes Bioscience
PrPs: Proteins with a purpose Lessons from the zebrafish
Edward Málaga-Trillo and Emily Sempou University of Konstanz; Department of Biology; Konstanz, Germany Corresponding author. Correspondence to: Edward Málaga-Trillo; Email: Edward.Malaga@uni-konstanz.deReceived April 28, 2009; Accepted July 29, 2009. Other Sections?
AbstractIntroduction
Breaking the “No Phenotype” Spell
The Road from Phenotype to Cellular FunctionImplications and Future DirectionsReferencesAbstractThe best-known attribute of the prion protein (PrP) is its tendency to misfold into a rogue isoform. Much less understood is how this misfolded isoform causes deadly brain illnesses. Neurodegeneration in prion disease is often seen as a consequence of abnormal PrP function yet, amazingly little is known about the normal, physiological role of PrP. In particular, the absence of obvious phenotypes in PrP knockout mice has prevented scientists from answering this important question. Using knockdown approaches, we previously produced clear PrP loss-of-function phenotypes in zebrafish embryos. Analysis of these phenotypes revealed that PrP can modulate E-cadherin-based cell-cell adhesion, thereby controlling essential morphogenetic cell movements in the early gastrula. Our data also showed that PrP itself can elicit homophilic cell-cell adhesion and trigger intracellular signaling via Src-related kinases. Importantly, these molecular functions of PrP are conserved from fish to mammals. Here we discuss the use of the zebrafish in prion biology and how it may advance our understanding of the roles of PrP in health and disease.
Key words: PrP, zebrafish, development, cell adhesion, signaling
Because of the genetic and functional complexities of the living embryo, we also have used a simplified cell culture assay to confirm that PrPs possess their own, intrinsic adhesive and signaling properties. Drosophila Schneider 2 (S2) cells lack endogenous PrP, do not express adhesion molecules, and therefore grow as single-cell suspensions. However, when we transfected them with mouse, zebrafish, frog or chicken PrP constructs, they acquired the ability to build cell clusters and accumulate PrP at cell-cell contacts. These effects were accompanied by the local accumulation of activated Src-kinases and tyrosine-phosphorylated proteins at cell-cell contact sites. Intriguingly, cell aggregation and intracellular signaling were also elicited among cells separately transfected with mouse and fish PrPs, revealing that PrP trans-interactions are very conserved and can take place even across a wide species range. If, as thought, PrP-mediated signals play a key role in prion pathogenesis, the observed interaction between fish and mammalian PrPs raises the need to assess whether exposure of fish to mammalian prions would lead to the generation of infectious fish prions.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802776/?tool=pubmed
WHAT has the feed industry done in the past about the TSE prion agent in feed ?
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
snip...
To minimise the risk of farmers' claims for compensation from feed compounders.
To minimise the potential damage to compound feed markets through adverse publicity.
To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.
snip...
THE FUTURE
4..........
MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.
5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.
6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...
SEE full text ;
http://collections.europarchive.org/tna/20080102153800/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf
THIS is what happens when you have the industry run the government $$$
Machine Vision Detection of Bonemeal in Animal Feed Samples
Authors: Nansen, Christian1; Herrman, Timothy2; Swanson, Rand3
Source: Applied Spectroscopy, Volume 64, Issue 6, Pages 158A-174A and 563-689 (June 2010) , pp. 637-643(7)
Publisher: Society for Applied Spectroscopy
Abstract:
There is growing public concern about contaminants in food and feed products, and reflection-based machine vision systems can be used to develop automated quality control systems. An important risk factor in animal feed products is the presence of prohibited ruminant-derived bonemeal that may contain the BSE (Bovine Spongiform Encephalopathy) prion. Animal feed products are highly complex in composition and texture (i.e., vegetable products, mineral supplements, fish and chicken meal), and current contaminant detection systems rely heavily on labor-intensive microscopy. In this study, we developed a training data set comprising 3.65 million hyperspectral profiles of which 1.15 million were from bonemeal samples, 2.31 million from twelve other feed materials, and 0.19 million denoting light green background (bottom of Petri dishes holding feed materials). Hyperspectral profiles in 150 spectral bands between 419 and 892 nm were analyzed. The classification approach was based on a sequence of linear discriminant analyses (LDA) to gradually improve the classification accuracy of hyperspectral profiles (reduce level of false positives), which had been classified as bonemeal in previous LDAs. That is, all hyperspectral profiles classified as bonemeal in an initial LDA (31% of these were false positives) were used as input data in a second LDA with new discriminant functions. Hyperspectral profiles classified as bonemeal in LDA2 (false positives were equivalent to 16%) were used as input data in a third LDA. This approach was repeated twelve times, in which at each step hyperspectral profiles were eliminated if they were classified as feed material (not bonemeal). Four independent feed materials were experimentally contaminated with 0-25% (by weight) bonemeal and used for validation. The analysis presented here provides support for development of an automated machine vision to detect bonemeal contamination around the 1% (by weight) level and therefore constitutes an important initial screening tool in comprehensive, rapid, and practically feasible quality control of feed materials.
Keywords: HYPERSPECTRAL IMAGING; QUALITY CONTROL; FEED INSPECTION; REAL-TIME ANALYSIS; BOVINE SPONGIFORM ENCEPHALOPATHY; PROHIBITED FEED CONTAMINANTS
Document Type: Research article
DOI: 10.1366/000370210791414335
Affiliations: 1: Texas AgriLife Research, 1102 E FM 1294 Lubbock, Texas 79403-6603; Plant and Soil Science Department, Texas Tech University, Campus Box 42122, Lubbock, Texas 79409 2: Office of the Texas State Chemist, Texas A&M, PO Box 3160, College Station, Texas 77841 3: Resonon Inc., 619 N. Church Ave. Suite 3, Bozeman, Montana 59715
http://www.ingentaconnect.com/content/sas/sas/2010/00000064/00000006/art00014?token=004e1715a3022dc7e41225f403842574767287d7667254549576b3427656c3c6a333f2566cf9f7
Tuesday, July 13, 2010
(SEE BEEF PRODUCTS EXPORTED TO AUSTRALIA FROM USA...TSS)
AUSTRALIAN QUESTIONNAIRE TO ASSESS BSE RISK (OIE) Terrestrial Animal Health Code, 2009 and USA export risk factor for BSE to Australia
http://usdameatexport.blogspot.com/2010/07/australian-questionnaire-to-assess-bse.html
Saturday, August 14, 2010
USA NON-SPECIES CODING SYSTEM (BEEF IMPORT EXPORT BSE RISK THERE FROM)
US denies it's illegally sending beef to Australia ?
Friday, 13/08/2010
http://usdameatexport.blogspot.com/2010/08/usa-non-species-coding-system-beef.html
Saturday, June 19, 2010
U.S. DENIED UPGRADED BSE STATUS FROM OIE
http://usdameatexport.blogspot.com/2010/06/us-denied-upgraded-bse-status-from-oie.html
Thursday, October 07, 2010
Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice
http://bse-atypical.blogspot.com/2010/10/experimental-transmission-of-h-type.html
Sunday, October 3, 2010
Scrapie, Nor-98 atypical Scrapie, and BSE in sheep and goats North America, who's looking ?
http://nor-98.blogspot.com/2010/10/scrapie-nor-98-atypical-scrapie-and-bse.html
TSS
About Me
- Terry S. Singeltary Sr.
- My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS
