TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU
© TAFS, Berne, 2010
Epidemiological evidence implicated contaminated rendered meat and bone meal as the source of the BSE epidemic in the United Kingdom, continental Europe as well as a few other countries around the world. With the overall global decline of BSE cases, national governments are beginning to explore the possibility of relaxing some of the measures taken to bring the disease under control. This paper will examine the current scientific knowledge and other facets that may impact decisions regarding the feed bans.
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Countries outside of Europe
After confirming BSE in September 2001, the government of Japan enacted many of the same regulations adopted by the European Union. In regard to feed controls, all meat and bone meal (MBM) is prohibited from being fed to bovines. Porcine and marine mammal derived MBM is banned from the rations of pigs and chickens as well. MBM from poultry produced separately may be fed to pigs and chickens. (Ref. 13)
These feed control measures appear to have been effective in Japan. Japan has detected a total of 36 cases of BSE (2001-2009) that seemingly peaked in 2006. In 2008 and 2009, only one case/year has been found. To date, with the exception of one case born in January 2002, all other BSE cases have been born prior to the feed ban.
BSE has also been identified in both Canada and the United States (US). The first case of BSE in Canada was reported in May 2003 and the first native-born case in the US was identified in 2004. Both Canada and the US prohibited the feeding of most rendered mammalian proteins to ruminants in 1997. It is evident by the Canadian BSE cases born between 2000-04 that this was not 100% effective.
In Canada as of July 12, 2007 SRMs (same list as removed from food for humans) are prohibited from being included in any animal feed including pet food or fertilizer.
As of October 2009, the US expanded the 1997 feed ban to prohibit the feeding of certain high risk cattle materials in all animal feed. This list includes: 1) the entire carcass of BSE-positive cattle, 2) the brains and spinal cords from cattle 30 months of age and older, 3) the entire carcass of cattle not inspected and passed for human consumption, unless the cattle are less than 30 months of age or the brains and spinal cords have been effectively removed, 4) tallow derived from BSE-positive cattle, 5) tallow derived from cattle material prohibited in animal feed (CMPAF) that contains more than 0.15% insoluble impurities and 6) mechanically separated beef derived from CMPAF.
Many countries not reporting BSE have taken some precautionary feed control measures to prevent an internal recycling of the BSE agent if it were to be introduced into the animal feed chain. The measures usually include a ruminant to ruminant or mammalian to ruminant ban. Some countries have also excluded SRMs from animal feed and set parameters for rendering. For example, as of 2001 Australia prohibits the feeding of any material taken from a vertebrate animal other than tallow, gelatin, milk products or oils extracted from poultry and fish. It includes rendered products such as blood meal, meat meal, meat and bone meal, fish meal, poultry meal, feather meal, and compounded feeds made from these products to be fed to ruminants. In 2002 Argentina enacted a mammalian to ruminant ban.
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Evaluation of these possible future developments
Disease considerations
In Europe there seems to be general support for the opinion that feeding any animal proteins to ruminants2 should remain forbidden to ensure that the BSE epidemic will not be revived and to respect the herbivorous nature of cattle and sheep. That particular feed ban was at the core of the hugely successful control of the BSE epidemic in Europe.
2 With the exception of fish meal in milk replacers
The inclusion of non-ruminant feed in the BSE feed ban regulations was not a result of a direct and proven TSE risk to, or arising from, non-ruminants, but rather the consequence of the complexity of the rendering and feed industry and the limited diagnostic capabilities.
Prior to the total feed ban, the production processes for ruminant and non-ruminant feed were not separated completely. During rendering processes, feed production, storage or transportation there was ample opportunity for ingredients of non-ruminant feed to contaminate ruminant feed and vice-versa. Despite previous feed bans, ruminant feed therefore continued to contain ruminant proteins, and crossfeeding of ruminants with non-ruminant feed containing ruminant proteins remained a possibility. The number of BSE cases born after ruminant-to-ruminant feed bans or mammalian-to-ruminant feed bans clearly demonstrates that in practice such feed bans were not sufficiently effective in preventing new infections. This was true for Europe and seems to be the same at least in Canada. Prior to finding the first case of BSE in Japan there was only a voluntary feed ban. After the initial case, Japan adopted more stringent and broader measures than the ruminant to ruminant or mammalian to ruminant ban.
While maintaining the total ban of PAPs in ruminant feed alone would in theory (e.g., under ideal, controlled conditions) be sufficient to protect cattle and sheep from exposure to potentially infected material, erroneous cross-contamination, labeling errors and fraudulent misconduct could lead to some contamination with PAPs in ruminant feed if they were to be allowed for non-ruminants. Inspections and testing (see below) can reduce, but not eliminate such a risk.
Even if PAPs would, unlawfully or unintentionally, end up in ruminant feed, they would pose no known TSE risk under the assumption of two important, jointly sufficient conditions:
1) That the PAPs stem exclusively from non-ruminants. With the complete ban of ruminant material being rendered into feed for farmed animals this assumption is very likely to be met, although pet feed could be a source of contamination.
2) That non-ruminant proteins can under no circumstances trigger the development of TSE diseases in ruminants even if fed to them. According to an EFSA opinion (Ref. 6) there is no evidence to suggest the contrary and EFSA considers the risk of transmitting BSE to pigs utilizing poultry PAPs (and vice versa) as negligible. On the other hand, there is also only weak evidence to actively support the scientific validity of this assumption. Additionally, pigs have been shown to be susceptible to infection with TSE-material of ruminant origin by parenteral challenge, but experimental transmission of BSE to pigs by the oral route has been unsuccessful (Ref 16). Given the current paucity of the experimental evidence, the condition cannot be considered completely satisfied, since the absence of evidence does not constitute evidence of absence.
No spontaneous development of TSE-like disease has been observed in pigs, but it is plausible to assume that pigs can develop such diseases as a very rare event and if left alive long enough. Multiplied by the number of live pigs – close to 1 billion worldwide – that would result in a non-negligible number of pigs with TSE. On the other hand by far most, if not all, pigs slaughtered for human consumption do not live to be even 1 year old.
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If pig-meal is allowed as feed to poultry and vice versa then a closed loop of material could be established provided that undigested pig proteins contained in the gastrointestinal tract of poultry is fed back to pigs or the other way round. This loop can be prevented if all gastrointestinal tracts and their contents are removed and discarded before the rendering of animal by-products. This requirement would be – like all other risk reduction measures – subject to error and fraud, but add to the redundancy of risk management.
In the light of the evolving BSE epidemic, the zoonotic potential of BSE and consumer concerns, the authorities were therefore forced to take drastic measures and exclude all animal proteins from all feed for farmed animals, with a few exceptions as outlined above.
By 2010, the BSE epidemic appears to be phasing out. In 2001, 2,167 BSE positive cases were detected within the framework of the EU surveillance activities. By 2008, this number had fallen to 125, 17 times less. Also the number of BSE cases detected per 10,000 animals tested had fallen dramatically: 2.55 BSE cases per 10,000 in 2001 against 0.12 BSE cases per 10,000 in 2008, a 21-fold reduction (Ref. 10). This also implies that the probability has diminished significantly that infected cattle erroneously enter the feed production chain.
Emerging Disease Considerations
Atypical BSE and other TSEs
For almost the entire two decades that BSE had been known in the world it was thought that there was only one ?train?that infected cattle and caused disease in other species such as humans (Refs. 17, 18).
In 2004, cases of a bovine prion disease molecularly different than those already documented as classical BSE were described by scientists in both Italy (Ref. 18) and France (Ref. 19). In both countries the cattle were over 8 years of age. The Italian cases (11 and 15 years of age) named bovine amyloidotic spongiform encephalopathy (BASE) were characterized by an unglycosylated protein band with a lower molecular mass (thus named L cases) and the predominance of the monoglycosylated band. In addition, immunohistochemical detection of PrPres in these cases found greater deposits in the cerebral cortex and thalamus versus the brain stem, as is characteristic of classical BSE. The French cases found a higher molecular mass associated with the unglycosylated protein band and were called H cases. The different ?trains?are now called atypical BSE.
Atypical BSE is a study in progress with more unknowns than knowns. One of the most important of the unknowns is the significance of atypical BSE in regard to human and animal health.
Since these two publications, additional cases of atypical BSE have been found in other countries. H cases have been detected in Canada, France, Germany, Japan, the Netherlands, Poland, Sweden, Switzerland, the United Kingdom and the United States. L cases have been diagnosed in Belgium, Canada, Denmark, France, Germany, Italy, Japan and Poland.
It has now been shown that both the L and H types of atypical BSE are experimentally transmissible via the intracerebral route. Homogenates from L cases have been transmitted to wild-type mice, bovinized, ovinized and humanized transgenic mice, Cynomolgus monkeys and cattle (Refs. 20, 21, and 22).
H cases have been transmitted to bovinized transgenic (Tgbov) and ovinized transgenic mice (Ref. 23) and cattle (personal communication March 2009).
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Early studies provide some evidence that L type (or BASE) BSE may be more virulent for primates including humans (Refs. 21, 24, and 25).
Studies on the oral route are underway. These would provide data to evaluate the potential for natural transmission of the disease.
Atypical BSE may arise spontaneously in a small proportion of cattle. The existence of sporadic CJD in humans has led to postulation that disease could arise spontaneously in any animal, but this theory like others has not been proved.
In the US one of the H-type BSE case was found to be associated with the novel mutation E211K within the prion protein gene (Prnp) suggesting that this strain may have a genetic origin (Ref. 26).
As per the SEAC: „here are too few data to enable an assessment of the natural transmissibility of L- and H-type BSE between cattle, or to sheep or goats. The present feed control measures which prevent feeding of mammalian meat and bone meal to ruminants would limit the spread of these forms of BSE to cattle, sheep and goats should they be transmissible to these species by the oral route.?
Atypical Scrapie
In 1998, scientists in Norway discovered a previously uncharacterized strain of scrapie that is now called Nor 98 or atypical scrapie (Ref. 27). Certain epidemiological evidence indicates that atypical scrapie may be a sporadic disease (Ref. 28), however additional research is underway to examine the likelihood of natural transmission and the extent of tissue distribution.
As with atypical BSE, there are few data on the potential for natural transmission of the disease to sheep and other species. The disease has been transmitted to sheep however the route was intracerebral (Ref. 29). Studies investigating the possibility of oral transmission are underway.
There is some evidence from transmission studies utilizing porcinized transgenic mice that pigs may be susceptible to atypical scrapie and BSE in sheep (Ref. 30). These studies do not involve the natural host or route of transmission so caution may be taken in drawing conclusions.
Potential for TSEs in Other Species
Studies conducted at the National Institutes of Health Rocky Mountain Laboratory caution against assuming that animals which do not become clinically ill are not infected. There is experimental evidence to indicate that certain species may become carriers (i.e., become infected, shed agent but do not progress to clinical disease) (Ref 31, Ref 32, Ref 33). Specifically, mice inoculated with 263K hamster scrapie demonstrated a phase of inactive persistence. That is, after exposure the mice had a prolonged period (approximately one year), where there was no evidence of infectivity or PrPsc. This was followed by a period of an increasing infectivity and agent adaptation. Many of the mice continued to be devoid of detectable PrPsc.
It is important to determine if this persistence and adaptation could occur naturally as it may have significance in feeding programs which continually expose species other than ruminants
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to TSE infectivity. The results of Race and colleagues, warns that an inactive persistent phase might not produce detectable PrPsc, yet tissues may harbor infectivity (Ref 32).
Very recent research provides illustrations of the accumulation of infectivity in tongue and nasal mucosa from terminally diseased field cases and experimentally challenged cases of BSE even when no abnormal PrP was detectable (Ref 34). This same phenomena has also been reported for peripheral tissues collected from sheep with atypical scrapie. (Ref 35).
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Key issues to deal with before the feed ban for non-ruminants can be relaxed
In our opinion, several key requirements need to be met before the feed ban for non-ruminants can be relaxed:
The feed industry needs to ensure the following:
Ruminant materials remain excluded completely from the entire feed chain. This requires a complete and reliable traceability system for both ruminant and non-ruminant materials.
Intra-species feeding is prevented entirely. This requires that pig and poultry by-products are prevented from mutual cross-contamination by dedicated separate logistical pathways from slaughterhouses through rendering and feed production processes.
No animal proteins are included in ruminant feed. This requires that the ingredients for and the production of ruminant feed is completely separate from the ingredients for and the production of non-ruminant feed.
Scientific knowledge required:
Diagnostic tools must be developed with the capacity to verify compliance with any revised feed ban. These tools must be able to differentiate between PAPs from different animal species, and – in case it is decided to implement a tolerance level for contamination of feed – they must be able to determine if the level of contamination exceeds the defined tolerance levels.
More research is needed to support the assumption that non-ruminant proteins cannot induce TSE-like diseases in ruminants, even if these diseases circulated among different non-ruminant species beforehand.
The authorities need to ensure the following:
Competent authorities have the means and capacity to monitor the feed industry closely and assess their capacity to comply with the remaining feed ban regulations BEFORE any changes are allowed to proceed.
Legislation is in place to hold the industry liable in case of breaches of the remaining feed ban.
Appropriate diagnostic tools are registered and validated to verify compliance with the feed regulations.
In the view of TAFS, taking into consideration all of the scientific and epidemiological knowns and unknowns, the fact that the requirements as listed above are currently not met and acknowledging the potential for fraudulent behavior, a relaxation of the feed ban at the present time would not eliminate all risks. We feel strongly that maintenance of the ban is the only means to drive the level of risk toward zero.
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see full text and references here ;
http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_ON_RELAXATION_OF_FEED_BAN_2010.pdf
PLEASE NOTE ***
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
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The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Atypical BSE in Cattle
BSE has been linked to the human disease variant Creutzfeldt Jakob Disease (vCJD). The known exposure pathways for humans contracting vCJD are through the consumption of beef and beef products contaminated by the BSE agent and through blood transfusions. However, recent scientific evidence suggests that the BSE agent may play a role in the development of other forms of human prion diseases as well. These studies suggest that classical type of BSE may cause type 2 sporadic CJD and that H-type atypical BSE is connected with a familial form of CJD.
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
snip...see full text ;
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America
update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS
THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) 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
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
please see full text ;
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Tuesday, March 2, 2010
Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA
http://madcowfeed.blogspot.com/2010/03/animal-proteins-prohibited-in-ruminant.html
Monday, March 1, 2010
ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010
http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html
Tuesday, September 14, 2010
Feed Safety and BSE/Ruminant Feed Ban Support Project (U18)
http://madcowfeed.blogspot.com/2010/09/feed-safety-and-bseruminant-feed-ban.html
Friday, October 8, 2010
Scientific reasons for a feed ban of meat-and-bone meal, applicable to all farmed animals including cattle, pigs, poultry, farmed fish and pet food
http://madcowfeed.blogspot.com/2010/10/scientific-reasons-for-feed-ban-of-meat.html
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these countries.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
O.4.3
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany
Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).
Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.
Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.
P.4.23
Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.
Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time. The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice.
BSE-H is also transmissible in our humanized Tg mice.
The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
P03.137
Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC
Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan
Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPSc. Severe spongiform change in the brain together with heavy accumulation of PrPSc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPSc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPSc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPSc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at not only CNS but also widely distributed lymphatic tissues.
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf
it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
http://www.usda.gov/oig/webdocs/sarc070619.pdf
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program  Phase II and Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
THIS is what happens when industry runs government policy ;
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/20090114060225/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf
Sunday, October 31, 2010
Scientific Opinion on the results of the EU survey for Chronic Wasting Disease (CWD) in cervids EFSA Panel on Biological Hazards (BIOHAZ) (October) 2010
http://chronic-wasting-disease.blogspot.com/2010/10/scientific-opinion-on-results-of-eu.html
Friday, October 15, 2010
BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle
http://bseusa.blogspot.com/2010/10/bse-infectivity-in-absence-of.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
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report
http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html
IBNC
"All of the 15 cattle tested showed that the brains had abnormally accumulated prion protein."
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009
SEAC 102/2
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
SEE where sporadic cjd in the USA went from 59 cases in 1997, to 216 cases in 2009. a steady increase since 1997. ...TSS
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1997 114 68 59 9 0 0
to
2009 425 259 216 43 0 0
http://www.cjdsurveillance.com/pdf/case-table.pdf
see full text ;
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
Wednesday, August 18, 2010
Incidence of CJD Deaths Reported by CJD-SS in Canada as of July 31, 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/08/incidence-of-cjd-deaths-reported-by-cjd.html
REPORT OF THE WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY 1989
snip...
4.2.9 ...Also, if it resulted from a localised chance transmission of the scrapie strain from sheep to cattle giving rise to a mutant, a different pattern of disease would have been expected: its range would have increased with time. Thus the evidence from Britain is against the disease being due to a new strain of the agent, but we note that in the United States from 1984 to 1988 outbreaks of scrapie in sheep flocks are reported to have Increased markedly, now being nearly 3 times as high as during any previous period (18).
http://collections.europarchive.org/tna/20080102132706/http://www.bseinquiry.gov.uk/files/ib/ibd1/tab02.pdf
http://collections.europarchive.org/tna/20080102193106/http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
Authors
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.
Content
Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.
The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.
Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross species barriers
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,
Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
PR-26
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS
R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway
Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.
*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
119
http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf
A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes
Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations
*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway
***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)
Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
http://www.pnas.org/content/102/44/16031.abstract
EU COMMENTS AND POSITIONS
On the proposed changes to OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals
20
CHAPTER 2.4.6: BOVINE SPONGIFORM ENCEPHALOPATHY
General comments
The changes proposed are generally welcomed by the EU. However, some specific comments detailed below should be taken into account for the final revised version to be adopted in the next General Session.
Specific comments
LINE 13: The words "and possibly spontaneous" should be added as follows: "... suggesting that earlier, undetected indigenous and possibly spontaneous cases may have occurred."
LINE 31: The EU would argue for the re-instatement of the deleted phrase [before, or without, the recognition] since fallen stock in particular could be showing some clinical signs which went unrecognised. As written, it applies more to the active screening of the healthy slaughter population.
Line 228: Replace: "All currently recognized forms of BSE (C, H and L-Type) are detectable by these methods." with: "Classical BSE is recognized by all these methods, while a complete evaluation of the approved BSE rapid tests on atypical forms (C, H and L-Type) was never carried out".
http://ec.europa.eu/food/international/organisations/docs/l410677%20EU%20positions%20OIE%2078GS%20Terrestrial%20Manual_annex.pdf
http://ec.europa.eu/food/international/organisations/docs/0510_general_session/Annex%20XXXV_scrapie%20EU%20position.pdf
http://ec.europa.eu/food/international/organisations/docs/0510_general_session/Annex%20XXVIII_BSE%20EU%20position.pdf
http://ec.europa.eu/food/international/organisations/EU_comments_position_papers_en.htm
SCRAPIE
http://www.oie.int/eng/normes/mcode/en_chapitre_1.14.9.htm
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html
Sunday, March 28, 2010
Nor-98 atypical Scrapie, atypical BSE, spontaneous TSE, trade policy, sound science ?
http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html
THE O.I.E. and it's junk science continues to emerge, and spread, and put the cart before the horse so to speak about atypical Scrapie with it's may and may not be risk factors, because all science to date shows that in fact the Nor-98 is a risk factor to not only animal health, but human health as well. SINCE when did the 'may not' and 'may' become sound science ?
"may not be contagious and may, in fact, be a spontaneous degenerative condition of older sheep’ (22)."
The OIE Terrestrial Animal Health Code (the Code) does not cover atypical scrapie/Nor 98 because, it states, the condition ‘… is clinically, pathologically, biochemically and epidemiologically unrelated to ‘classical’ scrapie, may not be contagious and may, in fact, be a spontaneous degenerative condition of older sheep’ (22).
22. World Organisation for Animal Health (OIE) (2009). – Terrestrial Animal Health Code. www.oie.int/eng/normes/mcode/en_chapitre_1.14.9.htm.
Last year, after examining member country submissions and investigating rigorous scientific research, the OIE (World Organisation for Animal Health) decided that atypical scrapie/Nor 98 should not be listed in its Terrestrial Animal Health Code. The Code sets out trade recommendations or restrictions for listed diseases or conditions, and the OIE determined there was no need for such recommendations around atypical scrapie/Nor 98.
http://www.biosecurity.govt.nz/files/pests/atypical-scrapie/atypical-scrapie-faq-oct09.pdf
Friday, May 7, 2010
Identification of atypical scrapie in Canadian sheep Brief Research Reports
http://nor-98.blogspot.com/2010/05/brief-research-reports-identification.html
Friday, August 27, 2010
NEW ATYPICAL NOR-98 SCRAPIE CASE DETECTED IDAHO NOW 5 CASES DOCUMENTED 2010
http://nor-98.blogspot.com/2010/08/new-atypical-nor-98-scrapie-case.html
Greetings,
(Figure 6) including five goat cases in FY 2008 that originated from the same herd in Michigan.
This is highly unusual for goats, and I strenuously urge that there should be an independent investigation into finding the common denominator for these 5 goats in the same herd in Michigan with Scrapie. ...
Kind Regards, Terry
Thursday, January 07, 2010
Scrapie and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010 and FISCAL YEAR 2008
http://scrapie-usa.blogspot.com/2010/01/scrapie-and-nor-98-scrapie-november.html
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html
TRANSMISSION OF SCRAPIE AND ATYPICAL SCRAPIE TO HUMANS, why not ?
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html
SEE FULL TEXT ;
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
Monday, December 21, 2009
Distinct Molecular Signature of Bovine Spongiform Encephalopathy Prion in Pigs
http://madporcinedisease.blogspot.com/2009/12/distinct-molecular-signature-of-bovine.html
Thursday, October 15, 2009
The presence of neurological signs in pigs inoculated with BSE without detectable PrPd raises the possibility that the BSE agent may produce a prion disease in pigs that remains undetected by the current postmortem tests.
Transmissibility studies of vacuolar changes in the rostral colliculus of pigs
http://madporcinedisease.blogspot.com/2009/10/transmissibility-studies-of-vacuolar.html
Saturday, December 01, 2007
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model Volume 13, Number 12–December 2007 Research
http://transmissible-mink-encephalopathy.blogspot.com/2007/12/phenotypic-similarity-of-transmissible.html
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html
Thursday, August 12, 2010
Seven main threats for the future linked to prions
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
WHAT ABOUT NORTH AMERICA ATYPICAL TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY, AND FRIENDLY FIRE, i.e. PASS IF FORWARD MODE OF TSE THERE FROM VIA BLOOD PRODUCTS AND OR TISSUE TRANSPLANT ;
PRODUCT
1) Plasma Frozen within 24 hours (FP24). Recall # B-2448-10;
2) Red Blood Cells. Recall # B-2449-10;
3) Cryoprecipitated AHF. Recall # B-2450-10;
4) Plasma. Recall # B-2451-10
CODE
1) Units: W038509802210, W038509800965;
2) Units: W038509802210, W038509800965, W038508801111, W038508330725;
3) Unit: W03850830725;
4) Units: W038509801111, W038508330725
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on July 9 and 21, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
9 units
DISTRIBUTION
Korea, SC, GA
___________________________________
PRODUCT
Recovered Plasma. Recall # B-2306-10
CODE
Unit: W137508110097
RECALLING FIRM/MANUFACTURER
Lane Memorial Blood Bank, Eugene, OR, by fax on June 10, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
KY
___________________________________
PRODUCT
Red Blood Cells (Apheresis) Leukocytes Reduced. Recall # B-2348-10
CODE
Units: W041609075327D (part a and b), 3922801 (part a and b)
RECALLING FIRM/MANUFACTURER
Blood Systems Inc/dba United Blood Services, Meridian, MS, by telephone and fax on May 26, 2010 and May 28, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
4 units
DISTRIBUTION
MS
___________________________________
PRODUCT
1) Recovered Plasma. Recall # B-2363-10;
2) Cryoprecipitated AHF, Pooled. Recall # B-2364-10;
3) Red Blood Cells Leukocytes Reduced. Recall # B-2365-10
CODE
1) and 3) Units: 2613522, 2578779;
2) Unit: 2578779
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax and e-mail on May 5, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
5 units
DISTRIBUTION
TX
___________________________________
END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm228605.htm
Friday, September 24, 2010
USA Blood products, collected from a donor who was at risk for vCJD, were distributed SEPTEMBER 2010
http://vcjdtransfusion.blogspot.com/2010/09/usa-blood-products-collected-from-donor.html
Enforcement Report for October 20, 2010
October 20, 2010
PRODUCT
1) Cryoprecipitated AHF. Recall # B-2523-10;
2) Plasma. Recall # B-2524-10;
3) Red Blood Cells. Recall # B-2525-10;
4) Fresh Frozen Plasma. Recall # B-2526-10
CODE
1) Unit: W038508310277;
2) Units: 3127765, W038508310277, 3129157, 4121927;
3) Units: W038508310277, 3129157, 3127765, 4025397, 4121927, 4018030;
4) Units: 4025397, 4018030
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by facsimile on July 22, 2010 and July 28, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
13 units
DISTRIBUTION
GA, MD, SC, Austria, Israel, South Korea, Switzerland
___________________________________
PRODUCT
1) Fresh Frozen Plasma. Recall # B-2531-10;
2) Recovered Plasma. Recall # B-2532-10;
3) Red Blood Cells Leukocytes Reduced. Recall # B-2533-10
CODE
1) Unit: W115910041730;
2) Units: W115910080008, W115910081199;
3) Units: W115910080008, W115910041730, W115910081199
RECALLING FIRM/MANUFACTURER
Central California Blood Center, Fresno, CA, by e-mail on July 19, 2010 and July 23, 2010 and by facsimile on July 23, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
6 units
DISTRIBUTION
Austria, CA
END OF ENFORCEMENT REPORT FOR OCTOBER 20, 2010
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm230357.htm
Enforcement Report for October 13, 2010
October 13, 2010
PRODUCT
1) Red Blood Cells Leukocytes Reduced. Recall # B-2275-10;
2) Recovered Plasma. Recall # B-2276-10;
3) Cryoprecipitated AHF, Pooled. Recall # B-2277-10
CODE
1), 2) and 3) Unit: 6400811
RECALLING FIRM/MANUFACTURER
South Texas Blood & Tissue Center, San Antonio, TX, by fax on April 7, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
3 units
DISTRIBUTION
FL, TX
___________________________________
PRODUCT
Fresh Frozen Plasma. Recall # B-2283-10
CODE
Units: W001606004574; W001606003405
RECALLING FIRM/MANUFACTURER
Department of the Air Force 88th Medical Group SGQC WPAFB, Wright Patterson, AFB, OH, by letter dated April 17, 2008. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who may have warranted deferral for residency in an area at risk for variant Creutzfeldt-Jakob Disease, were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
NJ
___________________________________
PRODUCT
1) Red Blood Cells Leukocytes Reduced. Recall # B-2322-10
2) Fresh Frozen Plasma. Recall # B-2323-10
CODE
1) and 2) Unit: W280310400336
RECALLING FIRM/MANUFACTURER
Upstate New York Transplant Services, Inc., Buffalo, NY, by telephone and fax on June 21, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
NY
___________________________________
PRODUCT
Red Blood Cells. Recall # B-2324-10
CODE
Unit: W121610120511
RECALLING FIRM/MANUFACTURER
The Blood Connection, Inc., Piedmont, SC, by fax and computerized notification system on June 17, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
NY
___________________________________
PRODUCT
Recovered Plasma. Recall # B-2325-10
CODE
Unit: W121610120511
RECALLING FIRM/MANUFACTURER
The Blood Connection, Inc., Piedmont, SC, by fax and computerized notification system on June 17, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
Switzerland
___________________________________
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm229271.htm
USA Blood products, collected from a donor who was at risk for vCJD, were distributed END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010
PRODUCT
1) Plasma Frozen within 24 hours (FP24). Recall # B-2448-10;
2) Red Blood Cells. Recall # B-2449-10;
3) Cryoprecipitated AHF. Recall # B-2450-10;
4) Plasma. Recall # B-2451-10
CODE
1) Units: W038509802210, W038509800965;
2) Units: W038509802210, W038509800965, W038508801111, W038508330725;
3) Unit: W03850830725;
4) Units: W038509801111, W038508330725
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on July 9 and 21, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
9 units
DISTRIBUTION
Korea, SC, GA
___________________________________
PRODUCT
Recovered Plasma. Recall # B-2306-10
CODE
Unit: W137508110097
RECALLING FIRM/MANUFACTURER
Lane Memorial Blood Bank, Eugene, OR, by fax on June 10, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
KY
___________________________________
PRODUCT
Red Blood Cells (Apheresis) Leukocytes Reduced. Recall # B-2348-10
CODE
Units: W041609075327D (part a and b), 3922801 (part a and b)
RECALLING FIRM/MANUFACTURER
Blood Systems Inc/dba United Blood Services, Meridian, MS, by telephone and fax on May 26, 2010 and May 28, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
4 units
DISTRIBUTION
MS
___________________________________
PRODUCT
1) Recovered Plasma. Recall # B-2363-10;
2) Cryoprecipitated AHF, Pooled. Recall # B-2364-10;
3) Red Blood Cells Leukocytes Reduced. Recall # B-2365-10
CODE
1) and 3) Units: 2613522, 2578779;
2) Unit: 2578779
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax and e-mail on May 5, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
5 units
DISTRIBUTION
TX
___________________________________
END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm228605.htm
Tuesday, September 28, 2010
Variant CJD: where has it gone, or has it?
Pract Neurol 2010; 10: 250-251
http://vcjdtransfusion.blogspot.com/2010/09/variant-cjd-where-has-it-gone-or-has-it.html
Monday, October 18, 2010
TSEAC Transmissible Spongiform Encephalopathies Advisory Committee Draft Agenda and Meeting Materials, Posted: 10/18/2010
http://tseac.blogspot.com/2010/10/tseac-transmissible-spongiform.html
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
http://tseac.blogspot.com/2010/09/transmissible-spongiform_14.html
Wednesday, September 08, 2010
Emerging Infectious Diseases: CJD, BSE, SCRAPIE, CWD, PRION, TSE Evaluation to Implementation for Transfusion and Transplantation September 2010
http://vcjdtransfusion.blogspot.com/2010/09/emerging-infectious-diseases-cjd-bse.html
layperson
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net
Saturday, November 6, 2010
Friday, October 8, 2010
Scientific reasons for a feed ban of meat-and-bone meal, applicable to all farmed animals including cattle, pigs, poultry, farmed fish and pet food
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.
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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-
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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.
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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
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.
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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-
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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.
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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
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