Greetings,
IF not so serious, it would almost be humorous, i.e. the EU is now saying
they can regulate PAPs, and keep them separated, ruminant from non-ruminant,
when they can’t even keep the horse meat and the donkey meat from mixing with
hamburger meat, i.e. I dubbed the EU horse and donkey gate burger meat scandal,
when in the past, the EU could not even distinguish between a cow brain and a
sheep brain. once again, big corporate ag and it’s junk science has won out over
sound science, and human and animal consumer will be the ones that suffer from
this, while the feed manufacturers are laughing all the way to the bank. ...TSS
EU Reauthorisation of non-ruminant processed animal proteins for fish feed
“EU feed industry acknowledges EU Commission decision as a significant step
to increase sustainability and competitiveness of EU aquaculture production”
(13) CP 5
Brussels, 24 January 2013
FEFAC President Patrick Vanden Avenne welcomed the European Commission
decision to adopt and publish the new regulation on the reauthorisation of
non-ruminant processed animal proteins exclusively for use for fish feeding. He
stated that “this measure paves the way for our EU aquaculture producers to step
up their efforts to encourage the sustainable development of EU aquaculture by
creating a level playing field with seafood imports from third countries”. “EFSA
has provided clear scientific evidence that non-ruminant PAPs produced in
accordance with the high EU processing standards are safe. They can help in
reducing the EU dependency on fishmeal imports thus contributing to the Common
Fisheries Policy reform goals of pairing sustainable wild fisheries with the
sustainable development of aquaculture”.
He highlighted that "the European feed industry is fully committed to
support the competitiveness and sustainability of aquaculture production in the
EU, as set out in the Commission proposal on the Common Fisheries Policy and
supported by the EP Committee on Fisheries in their December 2012 vote on the
CFP report of MEP Mrs Ulrike RODUST”. The new measure contributes to global food
security, by reducing the EU dependency on seafood imports which account for
more than 70% of the current EU consumption". He noted that PAPs are widely used
by aquaculture producers in Asia and North- and South-America, who are exporting
farmed fish to the EU.
Notes to the editor:
1. FEFAC, the European Compound Feed Manufacturers’ Federation, represents
22 national Associations in 21 EU Member States as well as Associations in
Switzerland, Turkey, Croatia, Serbia, Russia and Norway with observer/associate
member status. The European compound feed industry employs over 110,000 persons
on app. 4,000 production sites often in rural areas, which offer few employment
opportunities.
2. Farmed fish in the EU-27 consumes app.1.3 mio. t of fish feed a year.
Norway and Turkey produce another 1.6 mio. t of fish feed.
3. For more information see our web site (www.fefac.eu) or please contact
Alexander Döring, Secretary General Tel. +32-2-285.00.50, Fax +32-2-230.57.22,
e-mail: fefac@fefac.eu.
EU Allows Non-Ruminant Processed Animal Proteins for Fish Feed
February 13, 2013
In this week’s news, the European Commission has announced the
reauthorisation of non-ruminant processed animal proteins to be used for fish
feeding, helping to reduce the reliance on fishmeal imports and helping to boost
the sustainability of aquaculture, writes Lucy Towers, TheFishSite Editor.
European Feed Manufacturers’ Federation (FEFAC) President, Patrick Vanden
Avenne stated: “This measure paves the way for our EU aquaculture producers to
step up their efforts to encourage the sustainable development of EU aquaculture
by creating a level playing field with seafood imports from third
countries.”
Global feed company Nutreco has reported a strong year for 2012, with
revenue increasing by 10.8 percent to €5,229.1 (US$7,036.229) million. Some of
the company’s success was due to its 75 percent acquisition of the leading
shrimp and tilapia feed producer in Ecuador. The move took Nutreco into a global
top three position for shrimp feed.
Marine Harvest has also reported a major positive market shift in quarter
four of 2012, despite a huge decrease in profits compared to the year before,
caused partly by low salmon prices.
Salmon prices are now starting to look up, however. Alf-Helge Aarskog, CEO
of Marine Harvest commented: “I am very encouraged by the strong market outlook
in Europe, with future prices above NOK 30 (US$5.472) per kg for both 2013 and
2014. Marine Harvest is well positioned to take advantage of this as 80 percent
of our volume will be originating in Europe combined with high exposure to spot
prices.”
Chilean aquaculture experienced record harvests in 2012 of over one million
tons, according to preliminary figures released last week by the National
Fisheries and Aquaculture service, Sernapesca. Last week was also a good week
for fisheries in the EU as the European Parliament voted for an end to discards
and a move towards sustainable fishing.
The European Parliament voted 502 to 137 in favour of the draft report by
Ulrike Rodust, which sets out the basic regulations of the Common Fisheries
Policy reform package. The basic aim of the reform package is to create
sustainable fisheries, help fishing fleets to be economically viable and to
promote aquaculture in the EU.
Xavier Pastor, Executive Director of Oceana in Europe, said: “The EU took a
major step towards the proper management of our fishery resources. On behalf of
Oceana, I thank all the representatives of European citizens for backing
worldwide calls to act urgently for the health and future of our oceans.”
The Council of Fisheries ministers and the European Parliament will soon
start negotiations, along with the Commission, to reconcile their respective
positions and reach a final agreement on the reform by June 2013
In disease news, Infectious salmon anaemia (ISA) has been reported on a
salmon farm in Nordland, Norway and Viral Haemorrhagic Septicaemia was confirmed
on wrasse farms in Scotland, UK.
EU reauthorises non-ruminant PAP for fish feed
Process Managementpap
1120
The use of non-ruminant processing animal proteins (PAP) for use
exclusively for fish feed has been re-authorised by the European Commission last
week.
PAP has been prohibited since 2001 in response to the Bovine Spongiform
Encephalopath (BSE) epidemic.
Tracking and tracing systems will be implemented to ensure that at no stage
of the feed chain will cross-contamination occur with feeding-stuffs intended
for species other than fish. In addition, very sensitive analytical tests based
on DNA detection will be used to control the correct implementation of the
channelling system.
This re-authorisation will apply from 1 June 2013 and will improve the
overall sustainability of the aquaculture sector, since these PAPs could be a
valuable substitute for fishmeal.
FEFAC President Patrick Vanden Avenne welcomed the European Commission
decision to adopt and publish the new regulation on the reauthorisation of
non-ruminant processed animal proteins (PAP) exclusively for use for fish
feeding.
He stated that “this measure paves the way for our EU aquaculture producers
to step up their efforts to encourage the sustainable development of EU
aquaculture by creating a level playing field with seafood imports from third
countries”.
“EFSA has provided clear scientific evidence that non-ruminant PAPs
produced in accordance with the high EU processing standards are safe. They can
help in reducing the EU dependency on fishmeal imports thus contributing to the
Common Fisheries Policy reform goals of pairing sustainable wild fisheries with
the sustainable development of aquaculture”.
He highlighted that "the European feed industry is fully committed to
support the competitiveness and sustainability of aquaculture production in the
EU, as set out in the Commission proposal on the Common Fisheries Policy and
supported by the EP Committee on Fisheries in their December 2012 vote on the
CFP report of MEP Mrs Ulrike RODUST”. The new measure contributes to global food
security, by reducing the EU dependency on seafood imports which account for
more than 70% of the current EU consumption". He noted that PAPs are widely used
by aquaculture producers in Asia and North- and South-America, who are exporting
farmed fish to the EU.
by AllAboutFeed 18 Feb 2013
18 July 2012 – Member States voted by a qualified majority to accept a
proposal by the European Commission to allow pig and poultry processed animal
protein (PAP) to be incorporated into farmed fish feed. This measure is
currently expected to come into force in June 2013.
A total ban on Processed Animal Protein (PAP) in farmed livestock feed was
introduced in 2001 to reinforce earlier bans amid the BSE crisis. This was to
prevent cattle, sheep and goats from eating their own meat and bone meal via
contaminated feed – the way BSE spreads. However, BSE has declined dramatically,
with only 7 cases in the UK in 2011 (1 case to date in 2012), so the EU is
looking at ways to reduce unnecessary burdens on the industry.
The European Commission proposes to amend the current restrictions –
specifically, to allow pig and poultry processed animal protein (PAP) to be
incorporated into farmed fish feed. This follows the European Commission’s TSE
Roadmap 2 published in 2010 which considers various future policy options for a
managed relaxation in the TSE controls, whilst assuring a high level of food
safety and the protection of animal health. As a first step, the Commission
presented this specific proposal to Member States on 18 July, where it received
a qualified majority. This requires implementation of the new feed testing
regime which has just been developed across the EU.
The Government carefully considered the Commission’s proposal for the
inclusion of non-ruminant PAPs in fish feed and it recognises the importance of
risk based, proportionate policies, underpinned by good science and supports the
principles outlined in TSE Roadmap 2. However, it abstained from voting for the
Commission proposal, given that effective controls to prevent infective material
entering the food chain must be guaranteed, tests which can differentiate the
species of origin of PAP have only just been developed and consumer acceptance
of any change is expected to be low.
The proposal will now be subject to the Regulatory Procedure with Scrutiny,
which is expected to take three months from September, and will come into force
six months after it becomes law. At present, therefore, it is expected that this
measure will come into force in June 2013.
>>>Therefore it remains impossible to assess the risk of
transmitting a TSE by the mean of PAP that would derive from an Atypical BSE
case.<<<
SCIENTIFIC OPINION
Scientific Opinion on the revision of the quantitative risk assessment
(QRA) of the BSE risk posed by processed animal proteins (PAPs)1 EFSA Panel on
Biological Hazards (BIOHAZ)2, 3 European Food Safety Authority (EFSA), Parma,
Italy
snip...
4.4.3. Discussion of results
The results in Table 6 show that the estimated exposure for the assumed
contamination levels is very low indeed. The worst case, with atmospheric
processing of the ruminant Category 3 waste material and Intensive feeding of
cattle, gives a mean annual exposure of only 1.3 x 10-8 bovine oral ID50 units
per animal per year. This is assuming that the non-ruminant PAP could be
contaminated with up to 5% of ruminant PAP that had only been processed using
atmospheric methods that do not reduce BSE infectivity. This level of
contamination with ruminant material is extremely unlikely to occur. The
ruminant feed is then assumed to be contaminated with non-ruminant PAP at the
limit of detection (0.1%). Feed is routinely tested for the presence of
mammalian proteins and batches with positive results are rejected and not
allowed to be used for feed.
An exposure of 1.3 x 10-8 bovine oral ID50 units over a whole year is very
unlikely to result in any BSE infection. Even allowing for an uneven
distribution of infectivity in the feed these are very low levels indeed.
However, the occurrence of a very small number of cases cannot be excluded.
5.1. Conclusions on Atypical BSE
• Data are lacking concerning the pathogenesis, the origin (spontaneous
disorder/ contagious origin), the detection performances of the TSE
epidemiosurveillance system, the true prevalence and the ability of Atypical BSE
agents to be transmitted in cattle and other species after oral exposure.
• Some preliminary results seem to indicate that Atypical BSE infected
individual could be a potential source of Classical BSE agent.
• There are no data on the effect of the rendering process on the H- and L-
BSE infectivity level.
• In this context, the risk of Atypical BSE transmission through PAPs
cannot be assessed but should not be disregarded.
snip...
H- and L- BSE have been transmitted to inbred mice and Tg mice expressing
bovine and ovine PrP by intra-cerebral challenge. L-BSE has also been
transmitted to various models of transgenic mice expressing alleles of the human
prion protein (Beringue et al., 2007; Buschmann et al., 2006; Capobianco et al.,
2007). More recently the propagation of L-BSE (Fukuda et al., 2009; Lombardi et
al., 2008) in cattle through the intracerebral route was reported.
These results indicate that both Atypical BSE agents identified have the
potential capacity to propagate in different host species (including
cattle).
At this point there is no published information on:
• the transmissibility of Atypical BSE agents in cattle and other species
through the oral route;
• the distribution of the infectivity in peripheral tissues and body fluids
of cattle with H- and LBSE;
• the effect of the currently applied TSE agent inactivation process on the
H- and L-BSE agents. Therefore it remains impossible to assess the risk of
transmitting a TSE by the mean of PAP that would derive from an Atypical BSE
case.
Transmission and serial passage in inbred mice and Tg VRQ mice have been
interpreted to indicate that, after interspecies passage, L-BSE could generate
C-BSE (Beringue et al., 2007; Capobianco et al., 2007). However, it should be
noted that L-BSE : C-BSE phenotypic convergence has not observed in other Tg
mice, including mice expressing the ARQ allele of sheep PrP (Beringue et al.,
2007; Buschmann et al., 2006).
More recently transmission of H-BSE isolates originating from France and
Poland in Tg Bov was reported (Espinosa et al., 2010). While in the majority of
the cases the propagated TSE was different from Classical BSE, Classical BSE
have emerged in a proportion of the inoculated mice inoculated with two distinct
isolates (one from France and one from Poland). Together these data indicate
that the possibility that Atypical BSE might be a source of Classical BSE should
be considered with appropriate attention. 5.1. Conclusions on Atypical BSE
• Data are lacking concerning the pathogenesis, the origin (spontaneous
disorder/ contagious origin), the detection performances of the TSE
epidemiosurveillance system, the true prevalence and the ability of Atypical BSE
agents to be
transmitted in cattle and other species after oral exposure.
• Some preliminary results seem to indicate that Atypical BSE infected
individual could be a potential source of Classical BSE agent.
• There are no data on the effect of the rendering process on the H- and L-
BSE infectivity level.
• In this context, the risk of Atypical BSE transmission through PAPs
cannot be assessed but should not be disregarded.
CONCLUSIONS AND RECOMMENDATIONS
CONCLUSIONS
• The current global limit of detection for PAPs in feed is still
considered to be 0.1%.
• The EFSA 2004 QRA model was reviewed and compared with other published
similar risk assessments. The structure of the model is considered to be still
suitable for purpose of assessing the residual exposure from Classical BSE for
cattle posed by bovine derived processed animal proteins at European Union
level.
• For more specific questions and questions concerning particular
countries, a more specific or different model should be considered.
• An updated version of the EFSA 2004 QRA model was developed (called EFSA
QRA PAP model) to answer the specific terms of reference of this mandate.
• Scientific input data were reviewed and updated. Certain parameters were
considered to be conservative and uncertainties were identified.
• The EFSA QRA PAP model relies on the continuation of the current SRM
policy and TSE monitoring system. It also assumes that only Category 3 Animal
By-Product material is allowed to enter in PAP produced from ruminant
material.
• The EFSA QRA PAP model relies on the specific scenario described and on
specific assumptions like homogenous mixing. While conservative values are used,
uncertainties of certain parameters (i.e. the ratio of detected vs undetected
infected animals, the probability of incomplete SRM removal and the amount of
infectious tissue remaining after incomplete SRM removal) were identified.
Changes in scientific knowledge would require an adjustment of the model.
• The EFSA QRA PAP model calculations are based on the present available
data, including unofficial data about PAP production communicated directly by
industry. Changes in PAP and feed production would require adjustment of the
model input data.
• Based on 2009 BSE surveillance data and according to the EFSA QRA PAP
model, assuming a 0.1% contamination (which is the limit of detection for PAPs
in feed) with non-ruminant PAPs, the total BSE infectivity load that could enter
in cattle feed in the EU would be equivalent to 0.2 Co ID50 (9 x 10-5 – 1.3
CI95%) (that would mean that less than one additional BSE infected cattle could
be expected in the EU cattle population per year with an upper 95%
confidence).
• Considering the many uncertainties related to Atypical BSE L and H
(prevalence, tissue distribution of the infectious agent, efficacy of rendering
process for agent inactivation) the risk of Atypical BSE transmission through
PAPs cannot be assessed. It should however not be disregarded.
RECOMMENDATIONS
• In order to improve the limit of detection of animal proteins in feed the
development of analytical methods should be continued.
• Considering the limitations of the model (including the scenario and the
uncertainties), if the use of some mammalian PAPs for feeding animals should be
reintroduced the risk of (re-)emergence of TSEs in cattle should be taken into
account.
Fish models in prion biology: Underwater issues ☆
Edward Málaga-Trilloa, , 1, , Evgenia Saltab, 1, Antonio Figuerasc, Cynthia
Panagiotidisd, Theodoros Sklaviadisb, ,
a Department of Biology, University of Konstanz, 78457 Konstanz, Germany b
Department of Pharmacology, Aristotle University of Thessaloniki, 54124,
Thessaloniki, Greece c Instituto de Investigaciones Marinas, CSIC, 36208, Vigo,
Spain d Centre for Research and Technology-Hellas, Institute of
Agrobiotechnology, 57001, Thessaloniki, Greece
Abstract Transmissible spongiform encephalopathies (TSEs), otherwise known
as prion disorders, are fatal diseases causing neurodegeneration in a wide range
of mammalian hosts, including humans. The causative agents – prions – are
thought to be composed of a rogue isoform of the endogenous prion protein (PrP).
Beyond these and other basic concepts, fundamental questions in prion biology
remain unanswered, such as the physiological function of PrP, the molecular
mechanisms underlying prion pathogenesis, and the origin of prions. To date, the
occurrence of TSEs in lower vertebrates like fish and birds has received only
limited attention, despite the fact that these animals possess bona fide PrPs.
Recent findings, however, have brought fish before the footlights of prion
research. Fish models are beginning to provide useful insights into the roles of
PrP in health and disease, as well as the potential risk of prion transmission
between fish and mammals. Although still in its infancy, the use of fish models
in TSE research could significantly improve our basic understanding of prion
diseases, and also help anticipate risks to public health. This article is part
of a Special Issue entitled Zebrafish Models of Neurological Diseases.
Research Highlights
►Prion diseases may possibly be transmitted to fish species through the
food chain.
►Fish and mammalian PrPs share important cellular roles in cell–cell
communication.
►The use of zebrafish in prion research may help elucidating the role of
PrP in health and disease and also addressing TSE-related issues concerning
public health.
Fig. 3. Experimental transmission of prions between mammals and fish.
Inoculation of fish with ovine (A), bovine (B) and mouse (C) prions and their
various outcomes. The photographs on the upper right corner illustrate the
development of abnormal amyloid deposition in the optic tectum of BSE-challenged
sea bream, using the periodic acid Schiff (PAS) staining reaction. The right
image (scale bar = 10 μm) is a zoom-in of the lesion indicated in the left image
(scale bar = 100 μm). i.c., intracerebrally.
Abbreviations TSEs, transmissible spongiform encephalopathies; PrP, prion
protein; BSE, bovine spongiform encephalopathy; CJD, Creutzfeldt–Jakob disease;
GPI, glycosylphospatidylinositol; MBM, meat and bone meal; p.i., post
inoculation; i.c., intracerebrally; PK, proteinase K; GI, gastrointestinal
Keywords Prion protein; Transmissible spongiform encephalopathy;
Neurodegeneration; Fish; Zebrafish
Open AccessPeer-Reviewed Research Article
Evaluation of the Possible Transmission of BSE and Scrapie to Gilthead Sea
Bream (Sparus aurata)
Evgenia Salta equal contributor, equal contributor Contributed equally to
this work with: Evgenia Salta, Cynthia Panagiotidis
Affiliation: Department of Pharmacology, Aristotle University of
Thessaloniki, Thessaloniki, Greece
X Cynthia Panagiotidis equal contributor, equal contributor Contributed
equally to this work with: Evgenia Salta, Cynthia Panagiotidis
Affiliation: Centre for Research and Technology-Hellas, Institute of
Agrobiotechnology, Thessaloniki, Greece
X Konstantinos Teliousis, Affiliation: Laboratory of Pathology, School of
Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece
X Spyros Petrakis, Affiliations: Department of Pharmacology, Aristotle
University of Thessaloniki, Thessaloniki, Greece, Max Delbruck Center for
Molecular Medicine, Department of Neuroproteomics, Berlin-Buch, Germany
X Eleftherios Eleftheriadis, Affiliation: National Agricultural Research
Foundation, Fisheries Research Institute, Nea Peramos, Greece
X Fotis Arapoglou, Affiliation: National Agricultural Research Foundation,
Fisheries Research Institute, Nea Peramos, Greece
X Nikolaos Grigoriadis, Affiliation: B' Department of Neurology, AHEPA
University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece
X Anna Nicolaou, Affiliation: Department of Business Administration,
University of Macedonia, Thessaloniki, Greece
X Eleni Kaldrymidou, Affiliation: Laboratory of Pathology, School of
Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece
X Grigorios Krey, Affiliation: National Agricultural Research Foundation,
Fisheries Research Institute, Nea Peramos, Greece
X Theodoros Sklaviadi
Abstract
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-neuroprion.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.
snip...
The results of this TSE transmission study with gilthead sea bream indicate
the development of a CNS histopathology in the brains of the fish challenged
with the TSE-inocula. This neuropathology displays characteristics resembling a
novel fish amyloidosis more than a classical TSE. Specifically, while the fish
in our study showed no brain spongiosis and no clinical abnormalities, we did
find numerous plaque-like deposits in the brains of a significant proportion of
the BSE-challenged fish, especially. Although much of the PrP associated with
these deposits is PK-sensitive, this should not be taken as an indicator of low
potential infectivity, as instances of clinical prion disease, and even
infectivity, associated with extremely low levels of detectable PK-resistant PrP
have been reported [43]–[45].
In light of the serious ramifications that would follow an unequivocal
demonstration of prion disease transmission to fish, it must be emphasized here
that the abnormal deposition we observed in the brains of the TSE-challenged
fish could possibly have resulted from pathogenic factors other than the prions
they were fed. Despite the fact that no such naturally occurring, cross-species
infections from mammals to fish have ever been reported [46], we cannot
completely rule out this possibility. Thus, however unlikely, one must consider
the possibility that the brains used to prepare the inocula for the TSE
challenge were infected with an undetected virus or bacteria in addition to the
scrapie or BSE present. Together, the time course of brain lesion appearance,
i.e. months not days, the ability of the agent to survive the oral challenge
route, the absence of brain histopathology in any of the control groups and the
production of novel histological lesions in both the BSE- and the
scrapie-challenged fish, in the absence of inflammation, however, make this
possibility a remote one. A more plausible alternate explanation would be that
the amyloidogenic nature of the TSE-inocula might have contributed to the
development of a novel fish brain amyloidosis.
Infectivity and transmissibility are crucial issues that still need to be
addressed. From a public health standpoint, the transmissibility of each prion
strain and the relative ease with which it crosses species barriers, are its
most significant characteristics. The spectrum of prionopathies, which has
broadened in recent years, includes prion diseases that are not readily
transmissible (e.g. some GSS cases), prion strains often associated with
negligible clinical symptoms (e.g. the Nor98 scrapie strain), and even some
without detectable PrPSc (e.g. PSPr) [44], [47], [48]. It is clear, then, that
the evaluation and identification of both unusual prion diseases and prion
diseases affecting unusual hosts is a complex task, requiring lengthy studies of
pathogenesis, infectivity and transmissibility [49]. Until ongoing transmission
studies using “bovinized” transgenic mice are completed, the possibility that
the affected sea bream brain tissue might be infectious, must be taken seriously
in any consideration to lift EU feed bans, especially those related to farmed
fish.
TSE AND FISH
Evalution of the possible transmission of prions (scrapie and BSE) to
different fish species The pathogen common to all transmissible spongiform
encephalopathies (TSEs) is the 'prion', the major or sole component of which is
an abnormal glycoprotein (PrPSc). The 'benign' isomer of this protein is
normally expressed as cellular prion protein (PrPC), which is converted to its
pathological isoform. It is thought that, following oral ingestion, the
pathological form of the prion protein (PrPSc) can change the cellular form
(PrPC) to a pathological one. TSEs have been studied in higher organisms
including primates, rodents, etc, but little is known about TSE pathogenesis in
fish and lower vertebrates. However, fish farming is becoming a very important
industry, providing high protein nutrition. All farmed fish receive commercial
food containing 40-55% protein. Animal proteins may also be present and the
occurrence of the pathological protein cannot be excluded.
Objectives
The objectives of this proposal include the study of the effects produced
by oral administration of scrapie and BSE infectious material to trout, sea
bream and sea bass. It will include the evaluation of tissue lesions in these
fish species resulting from the primary transmission. As well, several tissue
homogenate samples from fish challenged with experimental mouse scrapie will be
used to evaluate any disease symptoms in recipient mice.
Molecular studies will allow the identification and characterisation of DNA
sequences encoding fish PrP and PrP-like proteins as potential targets necessary
for the transmission of TSEs in these lower vertebrates. Expression of
recombinant mature PrPs from fish species may allow antibody production and the
identification of markers for neuropathological disorders.
Progress to Date
Partner 1: Pilot studies indicate that the protocols developed for the TSE
pathogenesis studies in sea bream and sea bass are feasible.
Partner 2: Identification and cloning of two zebrafish cDNA sequences
encoding two distinct proteins exhibiting similarities to the prion protein
(PrP).Protein 1, called PrP-like protein and protein 2, called Shadoo, has been
accomplished.
Partner 3: Preliminary studies indicate that some residual infectivity is
observed in trout intestine taken one day after oral infectious. Some recipient
mice inoculated with brain and spleen of turbot resulted positive for scrapie.
Partner 4: Sequence information on PrP-like genes of Atlantic salmon have
been obtained.
lassified in ANIMALS, FISHERIES AND AQUACULTURE, HUMAN HEALTH AND
WELLBEING
Scientist responsible for the project Assoc. Prof. THEODOROS SKLAVIADIS 6th
Km CHARILAOU - THERMI ROAD Box 361 57001 THERMI - THESSALONIKI Greece - GR
References Project ID QLRT-2001-00866 Organisation CENTRE FOR RESEARCH AND
TECHNOLOGY - HELLAS / INSTITUTE FOR AGROBIOTECHNOLOGY Area 5.1.1 Start date 29
November 2002 Duration (months) 48 Total cost 2 058 876 € Total EC contribution
1 304 432 € Status Ongoing
The partners NORWEGIAN SCHOOL OF VETERINARY SCIENCES, Norway - NO
mohasina.syed@veths.no CENTRE FOR RESEARCH AND TECHNOLOGY - HELLAS / INSTITUTE
FOR AGROBIOTECHNOLOGY, Greece - GR sklaviad@pharm.auth.gr UNIVERSITA' DEGLI
STUDI DI MILANO, Italy - IT bolis@mailserver.unimi.it CONSEJO SUPERIOR DE
INVESTIGACIONES CIENTIFICAS, Spain - ES
pato1@iim.csic.es
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform
Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE,
or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or
another, but we have found that H-BSE can infect humans. I hope we could publish
these data once the study is complete. Thanks for your interest.''
Best regards,
Qingzhong Kong,
PhD Associate Professor Department of Pathology Case Western Reserve
University Cleveland, OH 44106 USA
END...TSS
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
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.
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.
P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN
HUMANIZED MOUSE MODELS
Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina
Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi
Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case
Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto
Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany;
4National Veterinary Research Institute, Poland; 5Kansas State University,
Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous
address: USDA National Animal Disease Center, Ames, IA 50010, USA
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). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have
been discovered in three continents since 2004. The first case of naturally
occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006
in the USA. The transmissibility and phenotypes of these atypical BSE
strains/isolates in humans were unknown. We have inoculated humanized transgenic
mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M
isolate. We have found that the atypical BSE-L strain is much more virulent than
the classical BSE-C.
*** The atypical BSE-H strain is also transmissible in the humanized
transgenic mice with distinct phenotype, but no transmission has been observed
for the BSE-M isolate so far.
III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE,
DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
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.
what about that ALABAMA MAD COW, AND MAD COW FEED THERE FROM IN THAT STATE
???
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
______________________________
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
###
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
###
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
###
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK
MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the
EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a
non-profit Swiss Foundation
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007 10 years (one decade) post August 4, 1997, partial and
voluntary mad cow BSE feed ban in the USA, nothing but ink on paper ;
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
Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
Thursday, February 14, 2013
Unique Properties of the Classical Bovine Spongiform Encephalopathy
Strain and Its Emergence From H-Type Bovine Spongiform Encephalopathy
Substantiated by VM Transmission Studies
Thursday, February 14, 2013
The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and
TSE prion disease
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2
December 2010
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
Thursday, December 23, 2010
Molecular Typing of Protease-Resistant Prion Protein in Transmissible
Spongiform Encephalopathies of Small Ruminants, France, 2002-2009
Volume 17, Number 1 January 2011
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans
Pecos
TSS
