California Firm Recalls Unwholesome Meat Products Produced Without the
Benefit of Full Inspection, what about the BSE TSE prion disease ?
From: Terry S. Singeltary Sr.
Sent: Saturday, February 08, 2014 8:53 PM
Subject: California Firm Recalls Unwholesome Meat Products Produced Without
the Benefit of Full Inspection ?
Greetings,
question please,
>>> California Firm Recalls Unwholesome Meat Products Produced
Without the Benefit of Full Inspection ?
‘’Without the Benefit of Full Inspection’’ ?
exactly what does this mean ?
I see this term in many recalls.
question please, could this include _any_ breaches that include _any_
potential risk factors for the Transmissible Spongiform Encephalopathy TSE Prion
disease when stipulated as ‘’Without the Benefit of Full Inspection’’ ?
kind regards, terry
California Firm Recalls Unwholesome Meat Products Produced Without the
Benefit of Full Inspection
Rancho Feeding Corporation, a Petaluma, Calif. establishment, is recalling
approximately 8,742,700 pounds, because it processed diseased and unsound
animals and carried out these activities without the benefit or full benefit of
federal inspection.
News Release California Firm Recalls Unwholesome Meat Products Produced
Without the Benefit of Full Inspection
Class I Recall 013-2014
Health Risk: High Feb 8, 2014
Congressional and Public Affairs Stacy Kish (202) 720-9113
WASHINGTON, Feb. 8, 2014 – Rancho Feeding Corporation, a Petaluma, Calif.
establishment, is recalling approximately 8,742,700 pounds, because it processed
diseased and unsound animals and carried out these activities without the
benefit or full benefit of federal inspection. Thus, the products are
adulterated, because they are unsound, unwholesome or otherwise are unfit for
human food and must be removed from commerce, the U.S. Department of
Agriculture’s Food Safety and Inspection Service (FSIS) announced today.
The following Rancho Feeding Corporation products are subject to
recall:
"Beef Carcasses” (wholesale and custom sales only)
2 per box "Beef (Market) Heads" (retail only)
4-gallons per box "Beef Blood" (wholesale only)
20-lb. boxes of “Beef Oxtail”
30-lb. boxes of “Beef Cheeks” 30-lb. boxes of " Beef Lips"
30-lb. boxes of "Beef Omasum" 30-lb. boxes of "Beef Tripas"
30-lb. boxes of "Mountain Oysters" 30-lb. boxes of "Sweet Breads”
30- and 60-lb. boxes of “Beef Liver” 30- and 60-lb. boxes of “Beef Tripe”
30- and 60-lb. boxes of “Beef Tongue”
30- and 60-lb. boxes of "Veal Cuts"
40-lb. boxes of "Veal Bones" 50-lb. boxes of “Beef Feet”
50-lb. boxes of “Beef Hearts”
60-lb. boxes of "Veal Trim" Beef carcasses and boxes bear the establishment
number "EST. 527" inside the USDA mark of inspection. Each box bears the case
code number ending in “3” or “4.” The products were produced Jan. 1, 2013
through Jan. 7, 2014 and shipped to distribution centers and retail
establishments in California, Florida, Illinois and Texas.
FSIS has received no reports of illness due to consumption of these
products. Anyone concerned about an illness should contact a health care
provider.
FSIS routinely conducts recall effectiveness checks to verify that
recalling firms notify their customers of the recall and that steps are taken to
make certain that recalled product is no longer available to consumers. When
available, the retail distribution list(s) will be posted on the FSIS website
at: www.fsis.usda.gov/recalls.
Consumers and members of the media who have questions about the recall can
contact the plant’s Quality Control manager, Scott Parks, at (707)
762-6651.
Consumers with food safety questions can “Ask Karen,” the FSIS virtual
representative available 24 hours a day at askkaren.gov. The toll-free USDA Meat
and Poultry Hotline 1-888-MPHotline (1-888-674-6854) is available in English and
Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through
Friday. Recorded food safety messages are available 24 hours a day. The online
Electronic Consumer Complaint Monitoring System can be accessed 24 hours a day
at: http://www.fsis.usda.gov/reportproblem.
USDA Recall Classifications Class I This is a health hazard situation where
there is a reasonable probability that the use of the product will cause
serious, adverse health consequences or death. Class II This is a health hazard
situation where there is a remote probability of adverse health consequences
from the use of the product. Class III This is a situation where the use of the
product will not cause adverse health consequences.
Last Modified Feb 08, 2014
>>> California Firm Recalls Unwholesome Meat Products Produced
Without the Benefit of Full Inspection ?
‘’Without the Benefit of Full Inspection’’ ?
exactly what does this mean ?
I see this term in many recalls.
question please, could this include _any_ breaches, that include _any_
potential risk factors for the Transmissible Spongiform Encephalopathy TSE Prion
disease when stipulated as ‘’Without the Benefit of Full Inspection’’ ?
kind regards, terry
Terry S. Singeltary Sr.
====================
*** UPDATE !!!
*** UPDATE !!!
Retail List for Recall Number: 013-2014, Various beef products
List Current As Of: 10-Feb-14
Retailer Name Street Address City State
1 Brown's Valley Market 3263 Browns Valley Rd. Napa CA-California
2 La Morenita 2436 Jefferson Napa CA-California
3 Vallergas Market 2139 1st St. Napa CA-California
4 Apple Market 155 San Marin Dr. Novato CA-California
5 Buds Meats 7750 Petaluma Hill Rd. Penngrove CA-California
6 G & G 701 Sonoma Mtn. Pkwy Petaluma CA-California
7 Petaluma Mkt. 210 Western Ave. Petaluma CA-California
8 Azteca Market 802 4th St. San Rafael CA-California
9 Carniceria Coalcoman 1415 Maple Ave. Santa Rosa CA-California
10 Carniceria Contreras 1401 Todd Rd. Santa Rosa CA-California
11 Carolina Wild 5380 Aero Dr. Santa Rosa CA-California
12 G & G 1211 W. College Ave. Santa Rosa CA-California
13 Willowside Meats 3421 Guernville Rd. Santa Rosa CA-California
14 Sonoma Market 500 W. Napa Sonoma CA-California
ORAL PRION INFECTION VIA CRANIAL NERVES
Sponsoring Institution
National Institute of Food and Agriculture
Project Status
TERMINATED Funding Source
NRI COMPETITIVE GRANT
Reporting Frequency
Annual
Accession No.0205803 Grant No.2006-35201-16626 Project No.MONB00436
Proposal No.2005-01901 Multistate No.(N/A) Program Code32.0Project Start DateDec
1, 2005 Project End DateNov 30, 2009 Grant Year2006 Project Director Bessen, R.
A. Recipient Organization MONTANA STATE UNIVERSITY (N/A) BOZEMAN,MT 59717
Performing Department Immunology & Infectious Diseases Non Technical
Summary
Prion diseases such as bovine spongiform encephalopathy in cattle, scrapie
in sheep, and chronic wasting disease in deer and elk, are caused by novel
infectious agents and results in a fatal degeneration of the central nervous
system. The goal of this research is to define the pathway of prion agent
infection of skeletal muscle following oral prion infection. Prion ingestion
establishes infection of lymphoid and nervous system tissues in the gut prior to
spread to the central nervous system. In this study, we will examine the ability
of the prion agent to spread from the brain to the tongue and infect skeletal
muscle and taste cells as well as the mechanism of prion agent entry into muscle
cells and the nervous system. These studies can improve our understanding of how
the prion agent spreads within a host in order to infect peripheral tissues such
as muscle. The findings from this study will be relevant to U.S. agriculture by
identifying 1) potential sites of prion agent infection in muscle and 2) the
ability of prions to infect the tongue, which is a food product. Animal Health
Component (N/A)Research Effort Categories
Basic100%Applied(N/A)Developmental(N/A)Classification
Knowledge Area (KA) Subject of Investigation (SOI) Field of Science (FOS)
Percent 311 3330 1103 25% 311 4099 1103 25% 712 3330 1103 25% 712 4099 1103 25%
Knowledge Area 311 - Animal Diseases; 712 - Protect Food from Contamination
by Pathogenic Microorganisms, Parasites, and Naturally Occurring Toxins;
Subject Of Investigation 4099 - Microorganisms, general/other; 3330 - Other
beef cattle products;
Field Of Science 1103 - Other microbiology;
Keywords
prion prion protein transmissible mink encephalopathy transmissible
spongiform encephalopathy oral infection ingestion tongue;
Goals / Objectives To investigate the centrifugal spread of the prion agent
from the brain stem to the tongue. To determine the route and mechanism of prion
agent infection of skeletal muscle and taste buds in the tongue during prion
disease. To examine the role of the neuromuscular junction in prion agent entry
and spread in nerves and skeletal muscle in the tongue. Project Methods The
chronological sequence of prion agent spread from the brainstem to the
peripheral nervous system and tongue following oral prion infection will be
determined. These studies will investigate the site(s) of prion agent
replication after exiting the brainstem and spread to the tongue. Nervous system
tissues, lymphoreticular tissues, and tongue will be collected each week and the
initial sites of prion agent replication will be determined by PrPSc detection.
To determine the route of prion entry into the tongue, prion infection will be
established in cranial nerves to the tongue and the sites of prion agent
deposition will be determined by PrPSc immunohistochemistry. To determine the
role of the neuromuscular junction in prion agent entry into skeletal muscle and
nerve fibers, unilateral axotomy of the hypoglossal nerve will be performed
prior to prion agent inoculation into the tongue. Prion agent infection will be
monitored over time in the tongue, ganglia and brainstem by PrPSc Western blot
and immunohistochemistry. Confocal microscopy will be performed to determine the
cellular and subcellular location of prion infection in the tongue of rodents
and sheep with prion disease. The latter studies will be performed in
collaboration with scientists at the National Animal Disease Center. Progress
12/01/08 to 11/30/09
Outputs The long-term goal of the proposed research is to define the route
and mechanism of prion agent infection of skeletal muscle during prion diseases
of livestock. The hypothesis to be tested is that prion neuroinvasion of the
brainstem following oral ingestion of the prion agent leads to infection of one
or more of the tongue-associated cranial nerves. In the past year we focused on
the following areas: 1) to determine if the prion agent can infect epithelial
cells at the mucosa and the route(s) of prion spread to epithelial mucosa, and
2) to investigate prion infection of tongue and nasal mucosa in ruminants with
prion disease. We continued our studies on the presence of prion infection in
tissues from the oral and nasal mucosa from ruminants with prion disease.
Greater than 80% of these mucosa-associated tissues were positive for PrP-res in
sheep with scrapie and deer and elk with chronic wasting disease. In cattle that
were infected with chronic wasting disease and transmissible mink
encephalopathy, PrP-res was not detected in tongue and nasal septal tissues.
These findings indicate that prion infection is present in mucosal tissues in
ruminant species in which horizontal transmission of prions (i.e., sheep and
cervids) is a common pathway of spread, but is not in these mucosal tissues of
cattle in which there is not an endemic prion disease. To measure prion
infection in epithelial cells at the oral mucosa, PrP-res deposition was
analyzed in the keratin layer of the stratified squamous epithelium (SSE) of
fungiform papillae and in the SSE of filiform papillae, which rarely contains
nerve fibers. Following infection of cranial nerves, we were able to detect
PrP-res in both the keratin layer of the SSE and the SSE of filiform papillae.
We were also able to demonstrate that PrP-res does colocalize with markers for
nerve fibers in these locations in some instances, but is also deposited in
areas without clear evidence of nerve fiber innervation. These studies strongly
suggest that epithelial cells in the oral mucosa can support prion infection and
shedding of the mucosa may be a source of prion infection in saliva.
Impacts The implication of these findings is that prion infection of muscle
and epithelium represents a potential source of prion transmission via either
consumption of meat products or from bodily fluids in contact with mucosal
epithelium, respectively. Nerve fibers that transverse almost all food products
are also a potential source of prion contamination of food. The prion
distribution into these sites in the tongue is likely via centrifugal spread
along motor and sensory fibers with subsequent transynatpic spread into muscle
cells or epithelial cells, respectively. These findings suggest that the prion
agent can use nerve fibers to spread to peripheral tissues and spread across
peripheral synapses to infect mucosal epithelium. This is the first study to
demonstrate prion spread via peripheral synapses into tissues. This conclusion
is also supported by in vitro studies that demonstrate the prion infection of
muscle cells in vitro required contact with neuronal cell lines and not
non-neuronal cells lines suggesting that a NMJ is required for prion infection
of muscle cells. Since the SSE of the tongue undergoes continual turnover,
renewal, and shedding, these findings suggest that the prion agent could
establish infection in epithelial cells and could be shed as these cells mature
in the SSE, become the keratinized layer, and are sloughed into oral bodily
fluids. Therefore, saliva may be one source of prions that is shed from a host
and can infect a naive host through direct or indirect contact. The spread of
prions into skeletal muscle cells via nerve fibers suggest that muscle tissue,
and not just nerves that transverse muscle, are a potential source of prion
exposure upon ingestion of food products containing meat.
Publications
Bessen, R.A., Martinka, S., Kelly, J., & Gonzalez, D. 2009. The role of
the lymphoreticular system in prion neuroinvasion from the oral and nasal
mucosa. Journal of Virology 83:6435-6445.
Progress 12/01/05 to 11/30/09
Outputs Outputs: The long-term goal of the proposed research is to define
the route and mechanism of prion agent infection of skeletal muscle during prion
diseases of livestock. The goals of this project were 1) to investigate the role
of peripheral synapses (e.g., neuromuscular junction) in prion infection of
skeletal muscle cells; 2) to establish prion infection in muscle cells in vitro;
3) to determine if the prion agent can infect epithelial cells at the mucosa and
the route(s) of prion spread to epithelial mucosa; and 4) to investigate prion
infection of tongue and nasal mucosa in ruminants with prion disease. To
investigate the role of the neuromuscular junction (NMJ) in prion entry into
skeletal muscle, a spatiotemporal analysis was performed on the deposition of
the disease-specific prion protein, PrP-res, in tongue following prion
infection. Our findings indicate that PrP-res colocalized with the NMJ at the
time of entry into skeletal muscle, but not later in the disease course. These
findings indicate that at the initial time of prion entry into cells that
PrP-res was linked to the NMJ, and suggests that this peripheral synapse acts as
a route for prion agent entry into muscle clls. To determine if skeletal muscle
cells can directly support prion infection, we attempted to establish prion
infection in a muscle cell line (C2C12 cells) in vitro. Scrapie infection of
murine C2C12 myoblasts and myotubes in vitro was established following
co-culture with a scrapie-infected murine neuroblastoma cell line, but not
following incubation with a non-neuronal cell line or a scrapie brain
homogenate. These in vitro studies also suggest that in vivo prion infection of
skeletal muscle requires contact with prion-infected neurons or, possibly, nerve
terminals. To determine if the prion agent can directly infect epithelial cells
at the tongue mucosa we analyzed the keratin layer of the stratified squamous
epithelium (SSE). PrP-res was detected in both the keratin layer of the SSE and
the SSE of filiform papillae. PrP-res did not always colocalize with markers for
nerve fibers in these locations suggesting infection was present in epithelial
cells. These studies strongly suggest that epithelial cells in the oral mucosa
can support prion infection and shedding of the mucosa may be a source of prion
infection in saliva. We investigated infection of tongue and nasal turbinates in
over 80 ruminants infected with prion diseases. In prion-infected sheep, deer,
and elk greater than 85% of tongue and nasal turbinates were PrP-res positive.
Tongue and nasal turbinates from CWD or TME-infected cattle were examined from
over 25 animals, but we were unable to detect PrP-res in any of these samples.
These findings indicate that prion infection is present in mucosal tissues in
ruminant species in which there is horizontal transmission of prions, but not in
cattle in which there is not an endemic prion infection.
Impacts The implication from these findings is that the prion agent can
spread away from the brain into mucosa tissues in the head, specifically the
tongue and nasal cavity. Since these tissues have a mucosal surface, it may be
possible that the prion agent is shed from the tongue or nasal cavity. In the
tongue, the epithelium is continually undergoing terminal differentiation and
shedding, and is then sloughed into saliva. In the nasal mucosa, olfactory
neurons continually mature and turnover during adult life and prions may be shed
from this mucosa into nasal secretions. Therefore, saliva and nasal secretions
may be a potential source of prions that are shed from a host and can infect a
naive host through direct or indirect contact. Another implication of these
findings is that prion infection of ruminant muscle is a potential threat to
animal and human food safety. The head of ruminants is banned for human or
ruminant consumption with the exception of the tongue. Our findings indicate
that prions undergo centrifugal spread from the brainstem to the tongue and can
enter skeletal muscle cells via the neuromuscular junction and further replicate
in muscle cells. These studies suggest that tongue should also be included in
the specified risk materials in order to minimize exposure to tongue products
containing prion agent.
Publications
DeJoia, C., Moreaux, B., O Connell, K. & Bessen, R.A. 2006. Prion
infection of oral and nasal mucosa. Journal of Virology 80:4546-4556. Dlakic,
W.M., Grigg, E. & Bessen, R.A. 2007. Prion infection of muscle cells in
vitro. Journal of Virology 81:4615-4624. (Faculty of 1000 Biology selection.)
Bessen, R.A., Martinka, S., Kelly, J., & Gonzalez, D. 2009. The role of the
lymphoreticular system in prion neuroinvasion from the oral and nasal mucosa.
Journal of Virology 83:6435-6445. Bessen, R.A., Shearin, H., Martinka, S.,
Boharski, R., Lowe, D., Wilham, J., Caughey, & Wiley, J. 2010. Prion
shedding from olfactory neurons into nasal secretions. PLoS Pathogens
6:e1000837.
Progress 12/01/07 to 11/30/08
Outputs The long-term goal of the proposed research is to define the route
and mechanism of prion agent infection of skeletal muscle during prion diseases
of livestock. Prion infection of skeletal muscle is a potential threat to animal
and human food products. The hypothesis to be tested is that prion neuroinvasion
of the brainstem following oral ingestion of the prion agent leads to infection
of one or more of the tongue-associated cranial nerves. In the past year we
focused on the following areas: 1) to investigate the role of peripheral
synapses (i.e., neuromuscular junction) in prion infection of skeletal muscle
cells, 2) to determine if the prion agent can infect epithelial cells at the
mucosa and the route(s) of prion spread to epithelial mucosa, and 3) to
investigate prion infection of tongue and nasal mucosa in ruminants with prion
disease. To investigate prion infection of oronasal tissues, we investigated
infection of tongue and nasal turbinates in >80 ruminant animals that were
experimentally infected with prion diseases. In prion-infected sheep, deer, and
elk greater than 85% of tongue and nasal turbinates were PrP-res positive. These
findings indicate that prion infection is present in mucosal tissues in ruminant
species in which there is horizontal transmission of prions (i.e., sheep and
cervids). To measure prion infection in epithelial cells at the oral mucosa,
PrP-res deposition was analyzed in tongue, specifically in the keratin layer of
the stratified squamous epithelium (SSE) of fungiform papillae and in the SSE of
filiform papillae, which rarely contains nerve fibers. Following infection of
cranial nerves, we were able to detect PrP-res in both the keratin layer of the
SSE and the SSE of filiform papillae. We demonstrated that PrP-res does
colocalize with markers for nerve fibers in these locations in most instances,
but is also located in the SSE in areas without clear evidence of nerve fiber
innervation. These studies strongly suggest that prions can invade epithelial
tissues via nerve fibers and may be able to enter or replicate in epithelial
cells in the oral mucosa. Prion localization to the oral epithelium has the
potential to result in the shedding of prions from the mucosa, which may be a
source of prion infection in saliva. We also continued to define the pathway by
which prions spread along cranial nerves of the tongue and the role of the
neuromuscular junction (NMJ) in prion entry into skeletal muscle. We initiated a
series of studies that examined prion infection of the hypoglossal nerve and
performed a spatiotemporal analysis of prion agent entry into the brainstem and
muscles of the tongue. Besides demonstating that prions likely enter the tongue
via the NMJ, we established that prions likely spread in axons will being
transported in organelles such as late endosomes, and can accumulate to high
levels in skeletal muscle. We are further investigating the location of prions
in axons in order to better understand how they move in the nervous system since
axonal spreading is one of the main pathways of prion dissemination throughout
the body of the host. These findings indicate that at the initial time of prion
entry into cells that PrP-res is linked to the NMJ and suggests that this
peripheral synapse acts as a route or prion agent entry into muscle cells. They
also suggest that prions can spread along axons into peripheral tissues.
Impacts The implication of these findings is that prion infection of muscle
and epithelium represents a potential source of prion transmission via either
consumption of meat products or from bodily fluids in contact with mucosal
epithelium, respectively. Nerve fibers transverse all bodily tissue and
therefore, almost all food products from an animal with subclinical prion
disease are a potential source of prion contamination of food. The prion
distribution into these sites in the tongue is likely via centrifugal spread
along motor and sensory fibers with subsequent transynatpic spread into muscle
cells or epithelial cells, respectively. These findings suggest that the prion
agent can use nerve fibers to spread to peripheral tissues and spread across
peripheral synapses to infect mucosal epithelium. This is the first study to
demonstrate prion spread via peripheral synapses into tissues. This conclusion
is also supported by in vitro studies that demonstrate the prion infection of
muscle cells in vitro required contact with neuronal cell lines and not
non-neuronal cells lines suggesting that a NMJ is required for prion infection
of muscle cells. Since the SSE of the tongue undergoes continual turnover,
renewal, and shedding, these findings suggest that the prion agent could
establish infection in epithelial cells and could be shed as these cells mature
in the SSE, become the keratinized layer, and are sloughed into oral bodily
fluids. Therefore, saliva may be one source of prions that is shed from a host
and can infect a naive host through direct or indirect contact. The spread of
prions into skeletal muscle cells via nerve fibers suggest that muscle tissue,
and not just nerves that transverse muscle, are a potential source of prion
exposure upon ingestion of food products containing meat.
Publications
Progress 12/01/06 to 11/30/07
Outputs The long-term goal of the proposed research is to define the route
and mechanism of prion agent infection of skeletal muscle during prion diseases
of livestock. Prion infection of skeletal muscle is a potential threat to animal
and human food products. The hypothesis to be tested is that prion neuroinvasion
of the brainstem following oral ingestion of the prion agent leads to infection
of one or more of the tongue-associated cranial nerves. In the past year we
focused on the following areas: 1) to investigate the role of peripheral
synapses (i.e., neuromuscular junction) in prion infection of skeletal muscle
cells, 2) to determine if the prion agent can infect epithelial cells at the
mucosa and the route(s) of prion spread to epithelial mucosa, and 3) to
establish prion infection in muscle cells in vitro. To investigate the role of
the neuromuscular junction (NMJ) in prion entry into skeletal muscle, the
hypoglossal motor nerve was inoculated with prions and a spatiotemporal analysis
was performed on the deposition of the disease-specific prion protein, PrP-res.
To determine the role of the NMJ in prion agent entry into muscle cells, laser
scanning confocal microscopy (LSCM) was used to determine the co-localization of
PrP-res with synaptophysin (a marker for the NMJ) at the initial time of entry
into muscle versus at the time of onset of clinical symptoms. We have now
demonstrated that PrP-res is statistically colocalized with the NMJ at the time
of entry into muscle cells, but not at later times in the disease course when
infection was widely distributed through muscle cells. These findings indicate
that at the initial time of prion entry into cells that PrP-res is linked to the
NMJ and suggests that this peripheral synapse acts as a route or prion agent
entry into muscle cells. Currently, we are investigating prion movement in nerve
bundles prior to entry into muscle cells to determine if this site is also
important for prion replication. To determine if skeletal muscles cells can
directly support prion infection, we have been able to establish prion infection
in a muscle cell line (i.e., C2C12 cells) in vitro. Scrapie infection of murine
C2C12 myoblasts and myotubes in vitro was established following co-culture with
a scrapie-infected murine neuroblastoma (N2a) cell line but not following
incubation with a non-neuronal cell line or a scrapie brain homogenate. These in
vitro studies also suggest that in vivo prion infection of skeletal muscle
requires contact with prion-infected neurons or, possibly, nerve terminals. This
study has now been published. To further determine if the prion agent can
directly infect epithelial cells at the tongue mucosa via cranial nerves, the
prion agent was inoculated into the sensory nerves of the tongue. This resulted
in early targeting of prion infection to the nerve fibers of the tongue. A high
level of prion infection was found in the sensory fibers and taste cells in
fungiform papillae of the tongue. We are currently investigating whether prions
can infect the epithelium of the oral mucosa and preliminary findings are
promising. These studies may suggest that epithelial cells in the oral mucosa
can support prion infection and shedding of the mucosa may be a source of prion
infection in saliva.
Impacts The implication of these findings is that prion infection of muscle
and epithelium represents a potential source of prion transmission via either
consumption of meat products or from bodily fluids in contact with mucosal
epithelium, respectively. The prion distribution into these sites in the tongue
is likely via centrifugal spread along motor and sensory fibers with subsequent
transynatpic spread into muscle cells or epithelial cells, respectively. These
findings suggest that the prion agent can use nerve fibers to spread to
peripheral tissues and spread across peripheral synapses to infect mucosal
epithelium. This is the first study to demonstrate prion spread via peripheral
synapses into tissues. This conclusion is also supported by in vitro studies
that demonstrate the prion infection of muscle cells in vitro required contact
with neuronal cell lines and not non-neuronal cells lines suggesting that a NMJ
is required for prion infection of muscle cells. Since the SSE of the tongue
undergoes continual turnover, renewal, and shedding, these findings suggest that
the prion agent could establish infection in epithelial cells and could be shed
as these cells mature in the SSE, become the keratinized layer, and are sloughed
into oral bodily fluids. Therefore, saliva may be one source of prions that is
shed from a host and can infect a naive host through direct or indirect contact.
The spread of prions into skeletal muscle cells via nerve fibers suggest that
muscle tissue, and not just nerves that transverse muscle, are a potential
source of prion exposure upon ingestion of food products containing meat.
Publications
Dlakic, W.M., Grigg, E. & Bessen, R.A. 2007. Prion infection of muscle
cells in vitro. Journal of Virology 81:4615-4624.
Progress 12/01/05 to 11/30/06
Outputs The long-term goal of the proposed research is to define the route
and mechanism of prion agent infection of skeletal muscle during prion diseases
of livestock. Prion infection of skeletal muscle is a potential threat to animal
and human food products. The hypothesis to be tested is that prion neuroinvasion
of the brainstem following oral ingestion of the prion agent leads to infection
of one or more of the tongue-associated cranial nerves. In the past year we
focused on the following aims: 1) to investigate the role of peripheral synapses
(i.e., neuromuscular junction) in prion infection of skeletal muscle cells and
2) to establish prion infection in muscle cells in vitro. To investigate the
role of the neuromuscular junction (NMJ) in prion entry into skeletal muscle, a
spatiotemporal analysis was performed on the deposition of the disease-specific
prion protein, PrP-res, in nerve fibers and muscle of the tongue, which we use
as a model for prion infection of skeletal muscle. To determine the role of the
NMJ in prion agent entry into muscle cells, laser scanning confocal microscopy
(LSCM) was used to determine the co-localization of PrP-res with synaptophysin
(a marker for the NMJ) at the initial time of entry into muscle versus at the
time of onset of clinical symptoms. Our early findings suggest that PrP-res is
colocalized with the NMJ at the time of entry into muscle cells but not later in
the disease course when PrP-res is widely distributed in skeletal muscle. These
preliminary findings suggest that prion agent entry into cells is linked to the
NMJ and suggests that this peripheral synapse acts as a route or prion agent
entry into muscle cells. To determine if skeletal muscles cells can directly
support prion infection, we attempted to establish prion infection in a muscle
cell line (i.e., C2C12 cells) in vitro. Scrapie infection of murine C2C12
myoblasts and myotubes in vitro was established following co-culture with a
scrapie-infected murine neuroblastoma (N2a) cell line but not following
incubation with a non-neuronal cell line or a scrapie brain homogenate. These in
vitro studies also suggest that in vivo prion infection of skeletal muscle
requires contact with prion-infected neurons or, possibly, nerve
terminals.
Impacts The implication of these findings is that prion infection of muscle
represents a potential source of prion transmission via either consumption of
meat products. The prion distribution into these sites in the tongue is likely
via centrifugal spread along motor and sensory fibers with subsequent
transynatpic spread into muscle cells or epithelial cells, respectively. These
findings suggest that the prion agent can use nerve fibers to spread to
peripheral tissues. Our conclusion is also supported by in vitro studies that
demonstrate the prion infection of muscle cells in vitro required contact with
neuronal cell lines and not non-neuronal cells lines suggesting that a NMJ is
required for prion infection of muscle cells. The spread of prions into skeletal
muscle cells via nerve fibers suggest that muscle tissue, and not just nerves
that transverse muscle, are a potential source of prion exposure upon ingestion
of food products containing meat.
Publications
Sunday, February 2, 2014
The Presence of Disease-Associated Prion Protein in Skeletal Muscle of
Cattle Infected with Classical Bovine Spongiform Encephalopathy
NOTE Pathology
SEE EXAMPLES OF TONGUE SRM TSE PRION
North Dakota Firm Recalls Whole Beef Head Products That Contain Prohibited
Materials Recall Release CLASS II RECALL FSIS-RC-023-2010 HEALTH RISK: LOW
Congressional and Public Affairs (202) 720-9113 Catherine Cochran
WASHINGTON, April 5, 2010 - North American Bison Co-Op, a New Rockford,
N.D., establishment is recalling approximately 25,000 pounds of whole beef heads
containing tongues that may not have had the tonsils completely removed, which
is not compliant with regulations that require the removal of tonsils from
cattle of all ages, the U.S. Department of Agriculture's Food Safety and
Inspection Service (FSIS) announced today.
Tonsils are considered a specified risk material (SRM) and must be removed
from cattle of all ages in accordance with FSIS regulations. SRMs are tissues
that are known to contain the infective agent in cattle infected with Bovine
Spongiform Encephalopathy (BSE), as well as materials that are closely
associated with these potentially infective tissues. Therefore, FSIS prohibits
SRMs from use as human food to minimize potential human exposure to the BSE
agent.
New York Firm Recalls Beef Carcass That Contains Prohibited Materials
Recall Release CLASS II RECALL FSIS-RC-003-2010 HEALTH RISK: LOW
Congressional and Public Affairs (202) 720-9113 Atiya Khan
WASHINGTON, January 15, 2010 - Jerry Hayes Meats Inc., a Newark Valley,
N.Y., establishment is recalling approximately 490 pounds of a beef carcass that
may not have had the spinal column removed, which is not compliant with
regulations that require the removal of spinal cord and vertebral column from
cattle over 30 months of age, the U.S. Department of Agriculture's Food Safety
and Inspection Service (FSIS) announced today.
Spinal cord and vertebral column are considered a specified risk material
(SRM) and must be removed from cattle over 30 months of age in accordance with
FSIS regulations. SRMs are tissues that are known to contain the infective agent
in cattle infected with Bovine Spongiform Encephalopathy (BSE), as well as
materials that are closely associated with these potentially infective tissues.
Therefore, FSIS prohibits SRMs from use as human food to minimize potential
human exposure to the BSE agent.
Wednesday, October 30, 2013
SPECIFIED RISK MATERIAL (SRM) CONTROL VERIFICATION TASK FSIS NOTICE 70-13
10/30/13
Tuesday, March 5, 2013
Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening
of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)
FDA believes current regulation protects the public from BSE but reopens
comment period due to new studies
Minnesota Firm Recalls Bone-In Ribeye That May Contain Specified Risk
Materials
Recall Release
CLASS II RECALL
FSIS-RC-024-2013 HEALTH RISK: LOW
Congressional and Public Affairs Atiya Khan (202) 720-9113
WASHINGTON, March 25, 2013 – Triple J Family Farms, a Buffalo Lake, Minn.
establishment, is recalling approximately 15,270 pounds of bone-in ribeye
products because the vertebral column may not have been completely removed,
which is not compliant with regulations that require the removal of vertebral
column in cattle 30 months of age or older, the U.S. Department of Agriculture's
Food Safety and Inspection Service (FSIS) announced today.
The products subject to recall are: [View Labels (PDF Only)]
Approx. 40-lb boxes of "BEEF B/I RIB," bearing any of the following case
codes: "91-R109H-C," "91-R109H-S," "91-R109H-C-SB," or "91-R109H-S-SB."
The products subject to recall bear the establishment number "EST.17466"
inside the USDA mark of inspection. The products were produced and packaged on
various dates between Feb. 8, 2013, and March 21, 2013, and were distributed to
an FSIS-inspected establishment in New York for further processing and
distribution.
The problem was discovered by FSIS during a routine specified risk material
(SRM) verification and may have occurred as a result of a recent change in the
company's carcass separation practices. Vertebral column is considered a SRM and
must be removed from cattle of 30 months of age or older in accordance with FSIS
regulations. SRMs are tissues that may contain the infective agent in cattle
infected with Bovine Spongiform Encephalopathy (BSE), as well as materials that
are closely associated with these potentially infective tissues. Therefore, FSIS
prohibits SRMs from use as human food to minimize potential human exposure to
the BSE agent. There is no indication that any of the cattle slaughtered
displayed any signs of BSE.
FSIS routinely conducts recall effectiveness checks to verify recalling
firms notify their customers of the recall and that steps are taken to make
certain that the product is no longer available to consumers.
Consumers with questions about the recall should contact the company's HR
and Office Manager, Kendra Williams, at (320) 833-2001. Media with questions
about the recall should contact the company's QA Manager, Russell Harris, at
(320) 833-0107.
Consumers with food safety questions can "Ask Karen," the FSIS virtual
representative available 24 hours a day at AskKaren.gov or via smartphone at
m.askkaren.gov. "Ask Karen" live chat services are available Monday through
Friday from 10 a.m. to 4 p.m. ET. The toll-free USDA Meat and Poultry Hotline
1-888-MPHotline (1-888-674-6854) is available in English and Spanish and can be
reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through Friday. Recorded
food safety messages are available 24 hours a day. The online Electronic
Consumer Complaint Monitoring System can be accessed 24 hours a day at:
www.fsis.usda.gov/FSIS_Recalls/ Problems_With_Food_Products/index.asp
#
see labels ;
Monday, March 25, 2013
Minnesota Firm Recalls Bone-In Ribeye That May Contain Specified Risk
Materials Recall Release CLASS II RECALL FSIS-RC-024-2013
Saturday, December 15, 2012
*** Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation period in cattle -- an update 5 December 2012
Saturday, December 21, 2013
**** Complementary studies detecting classical bovine spongiform
encephalopathy infectivity in jejunum, ileum and ileocaecal junction in
incubating cattle ****
Saturday, November 10, 2012
Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk
Materials Nov 9, 2012 WI Firm Recalls Beef Tongues
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK
MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM
WASHINGTON, October 17, 2009
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM
WASHINGTON, Oct 15, 2009
Thursday, June 26, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials
Tuesday, July 1, 2008
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
Friday, August 8, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
941,271 pounds with tonsils not completely removed
Saturday, April 5, 2008
SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings
Friday, October 15, 2010
BSE infectivity in the absence of detectable PrPSc accumulation in the
tongue and nasal mucosa of terminally diseased cattle
SPECIFIED RISK MATERIALS SRMs
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK
MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the
EU
Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND
FOOD SAFETY a non-profit Swiss Foundation
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject
PRO/AH/EDR>
Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)
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.
*** October 2009 O.11.3
*** Infectivity in skeletal muscle of BASE-infected cattle
Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1,
Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3,
Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5,
Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological
Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS
Torino, Italy; 5University of Verona, Italy
Background: BASE is an atypical form of bovine spongiform encephalopathy
caused by a prion strain distinct from that of BSE. Upon experimental
transmission to cattle, BASE induces a previously unrecognized disease phenotype
marked by mental dullness and progressive atrophy of hind limb musculature.
Whether affected muscles contain infectivity is unknown. This is a critical
issue since the BASE strain is readily transmissible to a variety of hosts
including primates, suggesting that humans may be susceptible.
Objectives: To investigate the distribution of infectivity in peripheral
tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice
expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and
i.p. with 10% homogenates of a variety of tissues including brain, spleen,
cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from
cattle intracerebrally infected with BASE. No PrPres was detectable in the
peripheral tissues used for inoculation either by immunohistochemistry or
Western blot.
Results: Mice inoculated with BASE-brain homogenates showed clinical signs
of disease with incubation and survival times of 175±15 and 207±12 days. Five
out of seven mice challenged with skeletal muscle developed a similar
neurological disorder, with incubation and survival times of 380±11 and 410±12
days. At present (700 days after inoculation) mice challenged with the other
peripheral tissues are still healthy. The neuropathological phenotype and PrPres
type of the affected mice inoculated either with brain or muscle were
indistinguishable and matched those of Tgbov XV mice infected with natural BASE.
Discussion: Our data indicate that the skeletal muscle of cattle
experimentally infected with BASE contains significant amount of infectivity, at
variance with BSE-affected cattle, raising the issue of intraspecies
transmission and the potential risk for humans. Experiments are in progress to
assess the presence of infectivity in skeletal muscles of natural BASE.
1: J Infect Dis 1980 Aug;142(2):205-8
*** Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
BABY FOODS
There are 4 brands available for a quick survey - Boots, Cow & Gate,
Heinz and Robinson.
None of the meat dishes included 'offal' in the ingredients.
Steak & Kidney and Beef and Oxtail did, however, include kidney and
oxtail.....
snip...
About the only item it seems many remain to be decided next week is what if
anything we say about offal in baby food. I enclose now in confidence the draft
as it stands at present concerning this aspect. It might be that no action is
recommened. On the other hand, the working party, PERSUADED BY THE ANIMAL
EVIDENCE THAT IMMATURE ANIMALS ARE MORE SUSCEPTIBLE TO INFECTION WITH THE AGENTS
OF SPONGIFORM ENCEPHALOPATHY, may make some recommendations either about
labelling or about banning offal in baby food.......
Heinz Baby Foods
WE guarantee that __________________ are free from offal OTHER THAN that
which is named in any product description and in particular contain no thymus,
brains, spinal chord, spleen, and intestine.
THE ONLY OFFALS USED IN __________________ ARE KIDNEY, LIVER, AND OXTAIL
when they are always identified on the lable, both in the product description
and in the list of ingredients.
PICTURE OF BABY FOOD JAR NAMED STEAK AND KIDNEY LUNCH
INGREDIENTS - WATER, BEEF, CARROTS, POTATOES, KIDNEY, MODIFIED CORN FLOUR,
SPLIT GREEN PEAS, FLOUR, TOMATO PUREE, LIVER, .....
snip...
ANOTHER PICTURE OF BABY FOOD JAR NAMED BEEF AND OXTAIL DINNER
ingredients listed also, but difficult to read, name self explanitory,
contains beef and OXTAIL...TSS
ANOTHER BABY FOOD JAR NAMED LIVER AND BACON DINNER, ingredients
listed
ANOTHER BABY FOOD JAR NAMED STEAK AND KIDNEY DINNER, ingredients
listed
ANOTHER BABY FOOD JAR NAMED BRAISED STEAK AND KIDNEY, ingredients
listed
ANOTHER BABY FOOD JAR NAMED LAMB AND LIVER CASSEROLE, NO INGREDIENTS LISTED
(WHAT ABOUT LAMB AND BSE ??? TSS)
2. The Southwood report recommended that baby foods manufactureres should
not use ruminant offal and thymus in baby foods. This was interpreted as any
offal listed in Schedule 2 Part 2 of the Meat Product Regulations. The
Committee, in effect, are advising the Ministry that ANY offal which carries ANY
risk of transmitting the BSE agent to baby foods should not be used in their
manufacture. The offal listed in Part 2 Schedule 2 of the MPSFPR is by NO MEANS
EXHAUSTIVE, and OTHER ORGANS EXIST e.g. ENDOCRINE AND PITUITARY GLANDS, which
are HIGH 'RISK' from the point of view of the presence of BSE or Scrapie agent.
Therefore I feel that any regulations should widen the scope of the definition
of offal to include any of these organs NOT mentioned in Part 2...
snip...
5. I had some reservations about TAILMEAT because of its close association
with the spinal cord.
They classify offals into two groups as follows:-
(i) Diaphragm, head meat (muscle only), heart, kideny, liver, pancreas,
tail meat, thymus, tongue.
(ii) Brains, feet, intestine, lungs, oesophagus, rectum, spinal cord,
spleen, stomach, texticles udder.
Group (i) can be used in ALL MEAT PRODUCTS AND CAN COUNT TOWARD THE MEAT
CONTENT OF THOSE PRODUCTS
Group (ii) can only be used in cooked meat products and cannot count
towards meat content.......
21 pages;
snip...see full text ;
Sunday, May 18, 2008
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
CONFIDENTIAL
CONFIRMED CASE OF CJD IN DAIRY FARMER
http://web.archive.org/web/20030513115653/http://www.bseinquiry.gov.uk/files/yb/1993/07/14003001.pdf
3. Neither Dr Will nor the CJD surveillance unit intend to disclose the
existence of this case or make any comment at present unless it attracts media
attention.
snip...
HUMAN CASE DETAILS CONFIDENTIAL
snip...
6. CJD IN FARMERS
The second annual report on CJD surveillance in the UK, which is about to
be published, gives occupational history details of 29 definite and probable CJD
cases recorded in people who had a history of employment at any time in
particular occupational groups of potential significance for the occurrence of
the disease. The 29 cases were amongst 95 diagnosed over a 3 year period: the
other 66 cases did not fall into such occupational groups.
These relevant details are:-
MEDICAL/PARAMEDICAL/DENTISTRY 7
ANIMAL LABORATORY 1
PHARMACEUTICAL LABORATORY 0
RESEARCH LABORATORY 0
FARMERS/VETERINARY SURGEONS 7
BUTCHERS/ABATTOIR WORKERS/OCCUPATION INVOLVING DIRECT CONTACT WITH ANIMAL
OR CARCASES 5
OCCUPATION INVOLVING ANIMAL PRODUCTS 9
snip... full text ;
http://collections.europarchive.org/tna/20080102155201/http://www.bseinquiry.gov.uk/files/yb/1993/07/19001001.pdf
Rocky Mountain oysters, mountain oysters, prairie oysters, Montana tendergroin
or swinging sirloin
POLICY IN CONFIDENCE
CJD AND FARMERS
1. The article in the Daily Mail of 12 August again raises the question of
a CAUSATIVE LINK BETWEEN BSE AND CJD. This follows the death of a second farmer
from CJD...
snip...
I am, however, concerned about how DH and MAFF would respont to public
concern generated if there are further CJD cases among farmers.
snip...
4. Unwelcome, though it maybe to the Tyrrell Committee, I think they must
be asked at their next meeting to give further thought to what they might advise
the Department and MAFF if ANOTHER FARMER (or TWO) DEVELOPS CJD. OR, if a
butcher or abattoir worker develops the disease.
5. Although the Committee were given plenty of advance warning about the
second farmer, they may NOT BE SO FORTUNATE NEXT TIME ROUND. Some Contingency
planning on the Committee's response to a further case of CJD in a farmer seems
essential. At the same time the Committee should consider if there is SPECIAL
RISK TO FARMERS, FOR EXAMPLE THEIR HISTORICAL HABIT OF CHEWING CATTLE NUTS, that
might be implicated. .....(oh my GOD...tss)
http://web.archive.org/web/20030513183927/http://www.bseinquiry.gov.uk/files/yb/1993/08/12002001.pdf
Ministers will note from this that experts are of the view, that there is
unlikely to be a direct link between the cases of BSE, and the occurance of CJD
in the farmer.
(NOTE CJD increasing over 3 years. ...TSS)
'AGE AT ONSET' is therefore likely to be a reflection of particulary
aetiological factors, about which, for sporadic CJD at least, much is yet
unknown. IT has therefore been suggested that examination of the f/d i/p of
other groups with TSE's, and comparison with that of CJD subsets might help to
elucidate aetiological mechanisms for sporadic CJD in particular; i.e. ALMOST A
REVERSAL OF THE ORIGINAL UNDERTAKING.
OCCUPATIONAL EXPOSURE TO BSE AND CJD
2. The Tyrrell Committee met on 7 October and the significance of the two
cases of CJD reported in dairy farmers who had BSE-affected animals on their
farms was discussed at some length, AS WERE THE IMPLICATIONS OF A THIRD (OR
FORTH) similar case.
3. The Committee were unable to identify any possible risk factors over and
above those that they had already considered, both in general and with
particular of TASTING THE FEED does continue but there was no consensus about
the value of advising farmers to discontinue this practice. Feed currently in
use does not pose a risk because of the ruminant-ruminant feed ban.
http://web.archive.org/web/20030326190512/http://www.bseinquiry.gov.uk/files/yb/1993/10/11001001.pdf
>>> Feed currently in use does not pose a risk
because of the ruminant-ruminant feed ban. ...LOL 
From: Terry S. Singeltary Sr. Sent: Sunday, December 15, 2013 8:15 PM To:
BSE-L@LISTS.AEGEE.ORG Subject: [BSE-L] FDA PART 589 -- SUBSTANCES PROHIBITED
FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE
DECEMBER 2013 UPDATE
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
OAI 2012-2013
OAI (Official Action Indicated) when inspectors find significant
objectionable conditions or practices and believe that regulatory sanctions are
warranted to address the establishment’s lack of compliance with the regulation.
An example of an OAI classification would be findings of manufacturing
procedures insufficient to ensure that ruminant feed is not contaminated with
prohibited material. Inspectors will promptly re-inspect facilities classified
OAI after regulatory sanctions have been applied to determine whether the
corrective actions are adequate to address the objectionable conditions.
ATL-DO 1035703 Newberry Feed & Farm Ctr, Inc. 2431 Vincent St.
Newberry SC 29108-0714 OPR DR, FL, FR, TH HP 9/9/2013 OAI Y
DET-DO 1824979 Hubbard Feeds, Inc. 135 Main, P.O. Box 156 Shipshewana IN
46565-0156 OPR DR, FL, OF DP 8/29/2013 OAI Y
ATL-DO 3001460882 Talley Farms Feed Mill Inc 6309 Talley Rd Stanfield NC
28163-7617 OPR FL, TH NP 7/17/2013 OAI N
NYK-DO 3010260624 Sherry Sammons 612 Stoner Trail Rd Fonda NY 12068-5007
OPR FR, OF NP 7/16/2013 OAI Y
DEN-DO 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO
81067 OPR RE, TH HP 2/27/2013 OAI N
CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR
FR, OF HP 11/26/2012 OAI Y
*** DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO
80631-9501 OPR RE, TH HP 10/12/2012 OAI N
Ruminant Feed Inspections Firms Inventory (excel format)
PLEASE NOTE, the VAI violations were so numerous, and unorganized in dates
posted, as in numerical order, you will have to sift through them for
yourselves. ...tss
SNIP...SEE FULL TEXT ;
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Monday, February 03, 2014
CREUTZFELDT-JAKOB DISEASE T.S.E. PRION U.K. UPDATE As at 3rd February 2014
Friday, August 16, 2013
*** Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and
Contaminated blood products induce a highly atypical prion disease devoid of
PrPres in primates
WHAT about the sporadic CJD TSE proteins ?
WE now know that some cases of sporadic CJD are linked to atypical BSE and
atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all
it’s sub-types $$$
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010 ***
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ???
Friday, January 10, 2014
*** vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial
type prion disease, what it ???
Monday, January 13, 2014
*** Prions in Variably Protease-Sensitive Prionopathy: An Update Pathogens
2013
Pathogens 2013, 2, 457-471; doi:10.3390/pathogens2030457
Wednesday, January 15, 2014
*** INFECTION PREVENTION AND CONTROL OF CJD, VCJD AND OTHER HUMAN PRION
DISEASES IN HEALTHCARE AND COMMUNITY SETTINGS Variably Protease-Sensitive
Prionopathy (VPSPr) January 15, 2014
Sunday, January 19, 2014
*** National Prion Disease Pathology Surveillance Center Cases Examined1 as
of January 8, 2014 ***
Wednesday, October 09, 2013
WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY, £41,078,281
in compensation REVISED
Thursday, January 23, 2014
Medical Devices Containing Materials Derived from Animal Sources (Except
for In Vitro Diagnostic Devices) [Docket No. FDA–2013–D–1574]
Thursday, February 06, 2014
Commons Science and Technology Committee announce new inquiry on blood,
tissue and organ screening Parliament exposure vcjd and blood risk while still
ignoring recent risks factors of sporadic CJD
Saturday, February 01, 2014
vCJD With Extremely Low Lymphoreticular Deposition of Prion Protein MAY NOT
HAVE BEEN DETECTABLE
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic
Creutzfeldt-Jakob Disease
PLEASE SEE ;
*** USDA Recall Classifications Class I This is a health hazard situation
where there is a reasonable probability that the use of the product will cause
serious, adverse health consequences or death. ***
*** Class I Recall 013-2014 ***
***Health Risk: High ***
WASHINGTON, Feb. 8, 2014 – Rancho Feeding Corporation, a Petaluma, Calif.
establishment, is recalling approximately 8,742,700 pounds, because it processed
diseased and unsound animals and carried out these activities without the
benefit or full benefit of federal inspection. Thus, the products are
adulterated, because they are unsound, unwholesome or otherwise are unfit for
human food and must be removed from commerce, the U.S. Department of
Agriculture’s Food Safety and Inspection Service (FSIS) announced today.
please see ;
Bovine Spongiform Encephalopathy BSE was only mentioned one time here in
all this report ???
Foreign animal diseases include bovine spongiform encephalopathy (BSE),
foot and mouth disease, rinderpest, African swine fever, hog cholera, contagious
bovine pleuropneumonia, and Teschen's disease. In most cases, VS will want the
animal held so they can examine it.
Abnormal Body Movement
Ante-mortem signs that indicate an animal may have a condition or disease
referenced in the regulations can be associated with body movement and action,
body position, condition, function, surfaces, discharges, and body odor. Some
examples of the signs associated with body movement, action and position
include:
1. Lameness or limping-sometimes the cause of lameness is rather obvious;
sometimes not.
2. Stiffness and pain-lameness may be caused by arthritis in one or more
joints.
3. Central Nervous System (CNS) diseases-certain diseases such as rabies
and listeriosis can affect the brain and CNS. The animal may appear extremely
nervous or restless, excessively anxious or upset, or stagger or circle.
4. Certain poisons and toxic residues that the animal has been exposed to
may cause abnormal movement and action, such as staggering or circling.
5. Depression or disinterest may be a sign that the animal is in a dying or
moribund state. A moribund animal may not respond to noises or other stimuli.
Animals in a moribund condition are not eligible for slaughter.
6. It is possible that an animal that is depressed or fails to respond
normally to stimuli could be under the influence of a tranquilizer. Tranquilized
animals are not eligible for slaughter. Tranquilizers and other drugs have
specific withdrawal periods that must elapse before the animal is eligible for
slaughter.
7. An animal may be disoriented and run into things or butt its head
against objects.
8. Animals may scratch excessively or rub their hide against objects.
Scratching and rubbing associated with hair loss may indicate that the animal
has lice or mange infestation. Scabies is a mange condition that is a reportable
disease. The PHV must report this condition to other health agencies. These
agencies may want to take skin scrapings from the animal to confirm the
diagnosis.
9. Animals may have muscle tremors or shivering, hold their head to one
side, or have any number of abnormal gaits.
10. Animals may strain and assume abnormal body positions. For example,
urinary or intestinal disorders may cause straining and abnormal positions such
as arching of the back, tucking in of the abdomen (stomach), and extending the
neck and tail.
11. An animal may have difficulty in rising or be unable to get up at all
or be standing but unable to walk (or ambulate). These animals may be recumbent
non-ambulatory or standing non-ambulatory for a variety of reasons ranging from
an injury to severe
Livestock Antemortem Inspection
3-21-13
Livestock Slaughter Inspection Training 12
illness or depression. All non-ambulatory livestock must be examined by the
PHV. The PHV may choose to examine these animals where they are rather that move
them to the U.S. Suspect pen to avoid unnecessary handling and pain or injury to
the animal. All cattle that are non-ambulatory when presented for ante-mortem
must be condemned.
What animals are USDA testing in the surveillance program? These are random
samples at slaughter, aren't they? No. USDA's BSE surveillance program is
specifically targeted to the population most likely to have the disease, if it
is present. This population is NOT clinically healthy animals that would be
presented for slaughter. Rather, it includes animals that have some type of
abnormality, such as central nervous system signs; non-ambulatory, or a
"downer"; emaciated; or died for unknown reasons. Because these animals would
not pass the required ante-mortem inspection requirements at slaughter for human
consumption, we collect the majority of our samples at facilities other than
slaughter facilities - at rendering or salvage facilities, on-farm, at
veterinary clinics or veterinary diagnostic laboratories. With this targeted
approach, we can monitor the presence of disease in the US cattle population in
a much more efficient and meaningful way. The key to surveillance is to look
where the disease is going to occur.
Does USDA need to increase surveillance in California after this finding?
As USDA progresses with the epidemiological investigation, we will review any
specific or unique risk factors that may be identified in California, and will
review our overall surveillance efforts in light of any such findings. However,
our current surveillance efforts have a good geographic representation across
the regions of the country and are designed to monitor the presence of disease
in the entire U.S. cattle population versus focusing on individual states or
regions.
KEY POINTS In addition to a stringent feed ban imposed by the Food and
Drug Administration in 1997 as well as the removal of all specified risk
material which could harbor BSE, USDA has a strong surveillance program in place
to detect signs of BSE in cattle in the United States. In fact, we test for BSE
at levels ten times greater than World Animal Health Organization standards. The
program samples approximately 40,000 animals each year and targets cattle
populations where the disease is most likely to be found. The targeted
population for ongoing surveillance focuses on cattle exhibiting signs of
central nervous disorders or any other signs that may be associated with BSE,
including emaciation or injury, and dead cattle, as well as non-ambulatory
animals. Samples from the targeted population are taken at farms, veterinary
diagnostic laboratories, public health laboratories, slaughter facilities,
veterinary clinics, and livestock markets. In addition, approximately 5,000
samples each year are collected from renderers and similar salvage facilities.
2 Methodology
2.1 Changes to the Base Case
The base case was revised as follows:
• Antemortem inspection – FSIS decreased the assumed probability that
animals with clinical signs of BSE would be detected at antemortem inspection
(Section 2.1.1)
snip...
2.1.1 Antemortem Inspection
Table 1 summarizes changes made to assumptions related to antemortem
inspection.
Assumption Old New
value value
Probability of detecting BSE signs in animals that have 95% 50% reached the
clinical stage of the disease – Ambulatory
Probability of detecting BSE signs in animals that have 85% 25% reached the
clinical stage of the disease – Non-ambulatory
- 3
FSIS has also included the following sensitivity analyses:
• Sensitivity 5 – Antemortem inspection – We make the antemortem inspector
less effective at identifying cattle with clinical BSE signs. The antemortem
inspector detects none of animals, regardless of ambulatory status.
- 6
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION
SERVICE
WASHINGTON, DC FSIS DIRECTIVE 10,400.1 4/11/13
SAMPLE COLLECTION FROM CATTLE UNDER THE BOVINE SPONGIFORM ENCEPHALOPATHY
(BSE) ONGOING SURVEILLANCE PROGRAM
I. PURPOSE
This directive provides FSIS inspection program personnel (IPP) with
instructions regarding the collection of brain samples for the Animal and Plant
Health Inspection Service’s (APHIS) Bovine Spongiform Encephalopathy (BSE)
ongoing surveillance program. Most of the instructions in this directive were
last issued in FSIS Notice 13-12. This directive includes new instructions for
the Office of Program Evaluation, Enforcement and Review (OPEER) Regional
Director, (RD) when he or she has been notified by the Office of Field
Operations OFO) District Office (DO) of a Central Nervous System (CNS) condemned
animal.
KEY POINTS:
• Sets out definition of collection procedures.
• Describes FSIS responsibilities related to approved alternative off-site
sample collection.
• Provides FSIS sample collection for cattle displaying CNS symptoms.
Friday, February 24, 2012
SAMPLE COLLECTION FROM CATTLE UNDER THE BOVINE SPONGIFORM ENCEPHALOPATHY
(BSE) ONGOING SURVEILLANCE PROGRAM 2/14/12
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)
Page 1 of 98
A policy
statement36 regarding BSE sampling of condemned cattle at slaughter plants
provided that effective June 1, 2004, FSIS would collect BSE samples for
testing: 1) from all cattle regardless of age condemned by FSIS upon ante mortem
inspection for CNS impairment, and 2) from all cattle, with the exception of
veal calves, condemned by FSIS upon ante mortem inspection for any other
reason.
snip...
FSIS Notice 28-04, dated May 20, 2004, informed FSIS personnel that, “FSIS
will be collecting brain samples from cattle at federally-inspected
establishments for the purpose of BSE testing.” The notice further states that,
“Cattle off-loaded from the transport vehicle onto the premises of the
federally-inspected establishment (emphasis added), whether dead or alive, will
be sampled by the FSIS Public Health Veterinarian (PHV) for BSE after the cattle
have been condemned during ante mortem inspection. In addition, cattle passing
ante mortem inspection but later found dead prior to slaughter will be condemned
and be sampled by the FSIS PHV.” 34 FSIS regulations do not specifically address
the designation of an establishment’s “official” boundaries; however, FSIS
Notices 29-04 (dated May 27, 2004) and 40-04 (dated July 29, 2004) make it clear
that FSIS inspection staff are not responsible for sampling dead cattle that are
not part of the “official” premises. 35 APHIS’ area office personnel stated that
it was their understanding that some establishments in the State were not
presenting cattle that died or were down on the transport vehicle to FSIS for
ante mortem inspection. The dead and down cattle were left in the vehicle, if
possible. In rare circumstances, dead cattle may be removed from the trailer by
plant personnel to facilitate the unloading of other animals. 36 A May 20, 2004,
Memorandum between the Administrators of APHIS and FSIS.
USDA/OIG-A/50601-10-KC Page 24
APHIS has the responsibility for sampling dead cattle off-loaded onto
plant-owned property that is adjoining to, but not considered part of, the
“official premises.37 FSIS procedures38 provide that “Dead cattle that are
off-loaded to facilitate the off-loading of live animals, but that will be
re-loaded onto the transport vehicle, are not subject to sampling by FSIS.
snip...see full text ;
FSIS, USDA, HARVARD REPLY TO SINGELTARY
From: Terry S. Singeltary Sr.
Sent: Saturday, February 08, 2014 8:53 PM
Subject: California Firm Recalls Unwholesome Meat Products Produced Without
the Benefit of Full Inspection ?
Greetings,
question please,
>>> California Firm Recalls Unwholesome Meat Products Produced
Without the Benefit of Full Inspection ?
‘’Without the Benefit of Full Inspection’’ ?
exactly what does this mean ?
I see this term in many recalls.
question please, could this include _any_ breaches that include _any_
potential risk factors for the Transmissible Spongiform Encephalopathy TSE Prion
disease when stipulated as ‘’Without the Benefit of Full Inspection’’ ?
kind regards, terry
California Firm Recalls Unwholesome Meat Products Produced Without the
Benefit of Full Inspection
Rancho Feeding Corporation, a Petaluma, Calif. establishment, is recalling
approximately 8,742,700 pounds, because it processed diseased and unsound
animals and carried out these activities without the benefit or full benefit of
federal inspection.
snip...see full text ;
Sunday,
February 9, 2014
California Firm Recalls Unwholesome Meat Products Produced Without
the Benefit of Full Inspection, what about the BSE TSE prion disease ?
kind regards,
terry
layperson...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
flounder9@verizon.net
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