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What Do We Feed to Food-Production Animals? OH MY GOD!

flounder

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greetings,

from farm to fork, a wide variety of food for thought. a disgusting and appalling review of what you are forced to eat via big industry. and as far as the recent OIE review of the USA BSE, i stand by my previous convictions, ''bought and paid for by your local cattle dealer''. you be the judge. ...TSS



What Do We Feed to Food-Production Animals? A Review of Animal Feed
Ingredients and Their Potential Impacts on Human Health


Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly Walker1
1Johns Hopkins Center for a Livable Future, Bloomberg School of Public Health, Baltimore, Maryland, USA; 2Maryland Institute for
Applied Environmental Health, College of Health and Human Performance, University of Maryland, College Park, Maryland, USA;
3Lisa Y. Lefferts Consulting, Nellysford, Virginia, USA


OBJECTIVE: Animal feeding practices in the United States have changed considerably over the past
century. As large-scale, concentrated production methods have become the predominant model for
animal husbandry, animal feeds have been modified to include ingredients ranging from rendered
animals and animal waste to antibiotics and organoarsenicals. In this article we review current U.S.
animal feeding practices and etiologic agents that have been detected in animal feed. Evidence that
current feeding practices may lead to adverse human health impacts is also evaluated.


DATA SOURCES: We reviewed published veterinary and human-health literature regarding animal
feeding practices, etiologic agents present in feed, and human health effects along with proceedings
from animal feed workshops.


DATA EXTRACTION: Data were extracted from peer-reviewed articles and books identified using
PubMed, Agricola, U.S. Department of Agriculture, Food and Drug Administration, and Centers
for Disease Control and Prevention databases.


DATA SYNTHESIS: Findings emphasize that current animal feeding practices can result in the presence
of bacteria, antibiotic-resistant bacteria, prions, arsenicals, and dioxins in feed and animal-based food
products. Despite a range of potential human health impacts that could ensue, there are significant
data gaps that prevent comprehensive assessments of human health risks associated with animal feed.
Limited data are collected at the federal or state level concerning the amounts of specific ingredients
used in animal feed, and there are insufficient surveillance systems to monitor etiologic agents "from
farm to fork."


CONCLUSIONS: Increased funding for integrated veterinary and human health surveillance systems
and increased collaboration among feed professionals, animal producers, and veterinary and public
health officials is necessary to effectively address these issues.


KEY WORDS: animal feed, animal waste, concentrated animal feeding operations, fats, human health
effects, nontherapeutic antibiotics, rendered animals, roxarsone, zoonoses. Environ Health Perspect
115:663–670 (2007). doi:10.1289/ehp.9760 available via http://dx.doi.org/ [Online 8 February 2007]


snip...


U.S. Animal Feed Production
The U.S. animal feed industry is the largest
producer of animal feed in the world (Gill
2004). In 2004, over 120 million tons of primary
animal feed, including mixes of feed
grains, mill by-products, animal proteins, and
microingredient formulations (i.e., vitamins,
minerals, and antibiotics) were produced in
the United States (Gill 2004). In the same
year, the United States exported nearly
$4 billion worth of animal feed ingredients
(International Trade Centre 2004).


snip...


Rendered animal products. In 2003, the
U.S. rendering industry produced > 8 million
metric tons of rendered animal products,
including meat and bone meal, poultry byproduct
meal, blood meal, and feather meal
(National Renderers Association Inc. 2005b).
Most of these products were incorporated into
animal feed. However, data concerning the
specific amounts of rendered animal protein
that are used in animal feed are difficult to
obtain because the information is neither routinely
collected at the federal or state level nor
reported by the rendering industry. The latest
available data, collected by the USDA in 1984,
estimated that > 4 million metric tons of rendered
animal products were used as animal
feed ingredients (USDA 1988). Oftentimes
these ingredients are listed on animal feed
labels as "animal protein products." Thus, it is
difficult to discern precisely which animal protein
products are included in a particular animal
feed product (Lefferts et al. 2006).
Animal waste. Another major animal
protein–based feed ingredient is animal
waste, including dried ruminant waste, dried
poultry litter, and dried swine waste (AAFCO
2004; Haapapuro et al. 1997). As with rendered
animal products, there are no national
data on the total amounts of animal waste
included in animal feeds, although some
states have collected limited data concerning
this practice. In 2003, it was estimated that
approximately 1 million tons of poultry litter
were produced annually in Florida, and an
estimated 350,000 tons of this litter were
available for use in feed (Dubberly 2003).
Yet, information concerning the precise
amount of this "available" poultry litter that
was actually incorporated into Florida animal
feed was unavailable.
Recycling animal waste into animal feed
has been practiced for > 40 years as a means of
cutting feed costs. However, the U.S. Food
and Drug Administration (FDA) does not offi-
cially endorse the use of animal waste in feed
and has issued statements voicing the agency's
concern about the presence of pathogens and
drug residues in animal waste, particularly
poultry litter (FDA 1998). In line with these
concerns, the AAFCO, an organization that
develops guidelines for the safe use of animal
feeds, advises that processed animal waste
should not contain pathogenic microorganisms,
pesticide residues, or drug residues that could
harm animals or eventually be detected in animal-
based food products intended for human
consumption (AAFCO 2004). Nonetheless,
these guidelines are not adequately enforced at
the federal or state level.


snip...


Table 1. Animal feed ingredients that are legally used in U.S. animal feeds. a
Origin, raw material Examples
Plant
Forage Alfalfa meal and hay, Bermuda coastal grass hay, corn plant, and soybean hay
Grains Barley, corn (organic and genetically modified), oats, rice, sorghum, and wheat
Plant protein products Canola meal, cottonseed cakes and meals, peanut meal, safflower meal, and
soybean (organic and genetically modified) feed and meal
Processed grain by-products Distillers products, brewers dried grains, corn gluten, sorghum germ cake and
meal, peanut skins, and wheat bran
Fruit and fruit by-products Dried citrus pulp, apple pomace, and pectin pulp
Molasses Beet, citrus, starch, and cane molasses
Miscellaneous Almond hulls and ground shells, buckwheat hulls, legumes and their
by-products, and other crop by-products
Animal
Rendered animal protein from Meat meal, meat meal tankage, meat and bone meal, poultry meal, animal
the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell
production animals and other meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal
animals digest from dead, dying, diseased, or disabled animals including deer and elk
Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and undried
processed animal waste products
Marine by-products Fish meal, fish residue meal, crab meal, shrimp meal, fish oil, fish liver and
glandular meal, and fish by-products
Dairy products Dried cow milk, casein, whey products, and dried cheese
Mixed
Fats and oils Animal fat, vegetable fat or oil, and hydrolyzed fats
Restaurant food waste Edible food waste from restaurants, bakeries, and cafeterias
Contaminated/adulterated food Food adulterated with rodent, roach, or bird excreta that has been heat
treated to destroy pathogenic organisms
Other
Antibiotics Tetracyclines, macrolides, fluoroquinolones, and streptogramins
By-products of drug manufacture Spent mycelium and fermentation products
Arsenicals Roxarsone and arsanilic acid
Other metal compounds Copper compounds and metal amino acid complexes
Nonprotein nitrogen Urea, ammonium chloride, and ammonium sulfate
Minerals Bone charcoal, calcium carbonate, chalk rock, iron salts, magnesium salts, and
oyster shell flour
Vitamins Vitamins A, D, B12, E, niacin, and betaine
Direct-fed organisms Aspergillis niger, Bacillus subtilis, Bifidobacterium animalis, Enterococcus
faecium, and yeast
Flavors Aloe vera gel concentrate, ginger, capsicum, and fennel
Enzymes Phytase, cellulase, lactase, lipase, pepsin, and catalase
Additives generally regarded Acetic acid, sulfuric acid, aluminum salts, dextrans, glycerin, beeswax, sorbitol,
as safe (GRAS) and riboflavin
Preservatives Butylated hydroxyanisole (BHA) and sodium bisulfite
Nutraceuticals Herbal and botanical products
Plastics Polyethylene roughage replacement
aData adapted from AAFCO (2004).


snip...


Antibiotics. The use of antibiotics in animal
feed is also a public health concern.
Antibiotics are administered at nontherapeutic
levels in feed and water to promote growth
and improve feed efficiency. This practice has
been shown to select for antibiotic resistance
in both commensal and pathogenic bacteria in
a) the animals themselves (Aarestrup et al.
2000; Bager et al. 1997; Gorbach 2001;
Wegener 2003); b) subsequent animal-based
food products (Hayes et al. 2003; White et al.
2001); and c) water, air, and soil samples collected
around large-scale animal feeding operations
(Chapin et al. 2005; Chee-Sanford et al.
2001; Gibbs et al. 2006; Jensen et al. 2002).
Although the use of nontherapeutic levels
of antibiotics in animal feed is approved and
regulated by the FDA (2004), there is no U.S.
data collection system regarding the specific
types and amounts of antibiotics that are used
for this purpose. In response to this significant
data gap, several estimates of nontherapeutic
antibiotic usage have been published based on
USDA livestock production data and FDA
antibiotic usage regulations. For example,
Mellon et al. (2001) estimated that as much as
60–80% of antibiotics produced in the United
States are administered in feed to healthy livestock
at nontherapeutic levels. Many of these
antibiotics are the same compounds that are
administered to humans in clinical settings,
and include tetracyclines, macrolides, streptogramins,
and fluoroquinolones (FDA 2004).
Additional information regarding the types
and amounts of antibiotics used in U.S. livestock
is available in AAFCO (2004), FDA
(2004), and Mellon et al. (2001).
Metals. Metal compounds are also administered
in animal feeds, and the compounds currently
added to both swine and poultry feeds
that are particularly concerning from a public
health perspective are organoarsenicals. The
most commonly used organoarsenical, roxarsone
(4-hydroxy-3-nitrobenzenearsenic-acid),
is administered to feeds at concentrations ranging
from 22.7 g/ton to 45.4 g/ton to promote
growth and improve feed efficiency (Chapman
and Johnson 2002). When used in combination
with ionophores, roxarsone also act as a cococcidiostat
to control intestinal parasites
(Chapman and Johnson 2002). Once roxarsone
is ingested by animals, the parent compound
can be degraded into inorganic arsenite
(AsIII) and inorganic arsenate (AsV) in animal
digestive tracts and animal waste (Arai et al.
2003; Stolz et al. 2007). Both AsIII and AsV are
classified by the U.S. Environmental Protection
Agency (U.S. EPA) as group A human carcinogens
(U.S. EPA 1998). Many other metallic
compounds are also mixed into feeds, including
copper, manganese, magnesium, and zinc compounds,
as well as metal amino acid complexes
(AAFCO 2004).


snip...


Table 2. Biological, chemical, and other etiologic agents detected in animal feed and their potential human health impacts.
Etiologic agent Examples Potential human health impacts References
Bacteria Salmonellaspp., E. coliO157:H7 Bacterial infections a Angulo 2004; Crump et al. 2002; Davis et al. 2003
Antibiotic-resistant E. faecium, E. coli, C. jejuni Antibiotic-resistant bacterial infections a Aarestrup et al. 2000; Dargatz et al. 2005;
bacteria b Schwalbe et al. 1999; Sorensen et al. 2001
Prions Causative agent of BSE vCJD c Gizzi et al. 2003; Smith 2003
Arsenicals Roxarsone, AsIII, AsV Increased human exposures to inorganic arsenic that may Chapman and Johnson 2002; Lasky et al. 2004
contribute to increases in cancer risk a
Mycotoxins Aflatoxins, ochratoxins, fumonisins, Increased human exposures to mycotoxins that may Bhat and Vasanthi 1999; Hussein and Brasel
trichothecenes contribute to increases in cancer and noncancer risks a 2001
Dioxins and dioxin-like PCDDs, PCDFs, PCBs Increased human exposures to dioxin-like compounds that Eljarrat et al. 2002; Fries 1995; Huwe and
compounds may contribute to increases in cancer and noncancer risks a Larsen 2005
vCJD, variant Creutzfeldt-Jakob disease.
aInsufficient data are available to fully understand the magnitude of potential human health impacts associated with contaminated animal feed. bIncludes antibiotic-resistant bacteria
initially present in animal feed due to contaminated feed ingredients, and antibiotic-resistant bacteria resulting from the nontherapeutic use of antibiotics in feed. cDomestically
acquired human cases of vCJD have not been documented in the United States.


snip...


In another study, 165 rendered animal
protein products originating from poultry, cattle,
and fish were sampled from a poultry feed
mill and tested for antibiotic-resistant bacteria
(Hofacre et al. 2001). Eighty-five percent of all
feed ingredients sampled contained bacteria
resistant to one or more of the following four
antibiotics: ampicillin, amoxicillin, clavulanic
acid, and cephalothin. Poultry meal and bone
and meat meal (nonpoultry) samples represented
the greatest number of feed ingredient
samples containing bacteria resistant to five or
more antibiotics (Hofacre et al. 2001).


Prions. In addition to bacteria, animal
feeds (in particular, cattle feeds) can be contaminated
with the infectious agent associated
with BSE (Gizzi et al. 2003). BSE, which is
commonly referred to as mad cow disease,
belongs to a group of progressively degenerative
neurologic diseases called transmissible
spongiform encephalopathies (TSEs) (Deslys
and Grassi 2005; Smith 2003). The causative
agent of TSEs is believed to be an infectious
proteinaceous entity called a prion, which is
composed largely of a protease-resistant misfolded
protein (PrPSc). Infectious prions can be
present in animal feed as a result of using rendered
animal products from diseased animals
as feed ingredients. Although prions may be
present in all body tissues of diseased animals,
it is generally acknowledged that prions accumulate
in highest concentrations in central
nervous system tissues (GAO 2002; Smith
2003) that are referred to as specified risk
materials (SRMs). As defined by the USDA
Food Safety Inspection Service (USDA
2005b), SRMs include the skull, brain, eyes,
parts of the vertebral column, spinal cord,
trigeminal ganglia, and dorsal root ganglia of
cattle > 30 months of age, as well as the tonsils
and distal ileum of all cattle. In 1997, the FDA
banned SRMs from use in cattle and other
ruminant feed (GAO 2002). Nonetheless,
SRMs were allowed to be incorporated into
feeds for nonruminants (including poultry),
and subsequent waste products from nonruminants
are still permitted in ruminant feeds
(USDA 2005b).
As of yet, there are no definitive tests for
BSE infectivity in live animals (before symptoms
appear) (Deslys and Grassi 2005; GAO
2002). However, a number of rapid screening
tests based on ELISA or Western blot analyses
have been approved for post-mortem BSE
testing in cattle. Currently, the USDA is conducting
a national BSE testing program; yet,
only high-risk cattle are included in the program
and there are no plans to test animal
feed samples (that could include animal protein
from asymptomatic rendered animals) in
this surveillance effort (USDA 2004). A variety
of tests do exist for the detection of animal
tissues (in general) in animal feed, including
microscopic analyses, polymerase chain reaction,
immunoassay analyses, and near infrared
spectroscopy (Gizzi et al. 2003); nonetheless,
these methods are not robust enough to distinguish
between bovine products that are permitted
in ruminant feeds (i.e., milk and
blood) and bovine products that are prohibited
from ruminant feeds (GAO 2002;
Momcilovic and Rasooly 2000).


snip...


Variant Creutzfeldt-Jakob disease.
Beyond bacterial infections, a chronic human
health risk that has been linked to animal
feeding practices is variant Creutzfeldt-Jakob
disease (vCJD), a novel human neurodegenerative
prion disease that is currently
untreatable and fatal (Collinge 1999). vCJD
was first described in 1995 in two teenagers in
the United Kingdom and was believed to be
caused by infection with the causative agent
of BSE or mad cow disease (Smith 2003).
Molecular strain-typing studies and experimental
transmission studies in mice published
in 1996 and 1997 confirmed that vCJD is
caused by the same prion strain that causes
BSE (Collinge 1999).
The primary routes of human exposure to
prions remain debatable; however, the most
likely route is through the ingestion of beef
derived from cattle that were infected when
rendered animal proteins from diseased cattle
were included in their feed. It is hypothesized
that the UK population may have experienced
the highest exposures to BSE from
1989 to 1990, when the incidence of BSE
was still increasing in cattle and specific bans
on high-risk rendered bovine products were
still being implemented (Collinge 1999).
From 1995 to 2002, there were 121 fatalities
out of 129 diagnosed cases in the United
Kingdom (Smith 2003). To date, domestically-
acquired human cases of vCJD have not
been identified in the United States.
However, since BSE was first identified in the
United States in 2003, the Centers for
Disease Control and Prevention (CDC) have
enhanced national surveillance for all types of
CJD in the United States through the analysis
of multiple cause-of-death data derived from
death certificates (CDC 2005). Active CJD
surveillance is also being implemented
through the Emerging Infections Programs
established in four sites across the United
States (CDC 2005).


snip...


Conclusions
Food-animal production in the United States
has changed markedly in the past century,
and these changes have paralleled major
changes in animal feed formulations. While
this industrialized system of food-animal production
may result in increased production
efficiencies, some of the changes in animal
feeding practices may result in unintended
adverse health consequences for consumers of
animal-based food products.
Currently, the use of animal feed ingredients,
including rendered animal products, animal
waste, antibiotics, metals, and fats, could
result in higher levels of bacteria, antibioticresistant
bacteria, prions, arsenic, and dioxinlike
compounds in animals and resulting
animal-based food products intended for
human consumption. Subsequent human
health effects among consumers could include
increases in bacterial infections (antibioticresistant
and nonresistant) and increases in the
risk of developing chronic (often fatal) diseases
such as vCJD.
Nevertheless, in spite of the wide range of
potential human health impacts that could
result from animal feeding practices, there are
little data collected at the federal or state level
concerning the amounts of specific ingredients
that are intentionally included in U.S.
animal feed. In addition, almost no biological
or chemical testing is conducted on complete
U.S. animal feeds; insufficient testing is performed
on retail meat products; and human
health effects data are not appropriately
linked to this information. These surveillance
inadequacies make it difficult to conduct rigorous
epidemiologic studies and risk assessments
that could identify the extent to which
specific human health risks are ultimately
associated with animal feeding practices. For
example, as noted above, there are insufficient
data to determine whether other human foodborne
bacterial illnesses besides those caused
by S. enterica serotype Agona are associated
with animal feeding practices. Likewise, there
are insufficient data to determine the percentage
of antibiotic-resistant human bacterial
infections that are attributed to the nontherapeutic
use of antibiotics in animal feed.
Moreover, little research has been conducted
to determine whether the use of organoarsenicals
in animal feed, which can lead to
elevated levels of arsenic in meat products
(Lasky et al. 2004), contributes to increases in
cancer risk.
In order to address these research gaps,
the following principal actions are necessary
within the United States: a) implementation
of a nationwide reporting system of the specific
amounts and types of feed ingredients of
concern to public health that are incorporated
into animal feed, including antibiotics, arsenicals,
rendered animal products, fats, and animal
waste; b) funding and development of
robust surveillance systems that monitor biological,
chemical, and other etiologic agents
throughout the animal-based food-production
chain "from farm to fork" to human
health outcomes; and c) increased communication
and collaboration among feed professionals,
food-animal producers, and veterinary
and public health officials.

REFERENCES



Sapkota et al.
668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health Perspectives




http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1867957&blobtype=pdf



CVM Update
May 18, 2007

May 2007 Update on Feed Enforcement Activities to Limit the Spread of BSE

To help prevent the establishment and amplification of Bovine Spongiform
Encephalopathy (BSE) through feed in the United States, the Food and Drug
Administration (FDA) implemented a final rule that prohibits the use of most
mammalian protein in feeds for ruminant animals. This rule, Title 21 Part
589.2000 of the Code of Federal Regulations, here called the Ruminant Feed
Ban, became effective on August 4, 1997.

The following is an update on FDA enforcement activities regarding the
ruminant feed ban. FDA's Center for Veterinary Medicine (CVM) has assembled
data from the inspections that have been conducted AND whose final
inspection report has been recorded in the FDA's inspection database as of
May 12, 2007. As of May 12, 2007, FDA had received over 53,000 inspection
reports. The majority of these inspections (around 68%) were conducted by
State feed safety officials, with the remainder conducted by FDA officials.
Inspections conducted by FDA or State investigators are classified to
reflect the compliance status at the time of the inspection based upon the
objectionable conditions documented. These inspection conclusions are
reported as Official Action Indicated (OAI), Voluntary Action Indicated
(VAI), or No Action Indicated (NAI).

An OAI inspection classification occurs when significant objectionable
conditions or practices were found and regulatory sanctions are warranted in
order to address the establishment's lack of compliance with the regulation.
An example of an OAI inspection classification would be findings of
manufacturing procedures insufficient to ensure that ruminant feed is not
contaminated with prohibited material. Inspections classified with OAI
violations will be promptly re-inspected following the regulatory sanctions
to determine whether adequate corrective actions have been implemented.

A VAI inspection classification occurs when objectionable conditions or
practices were found that do not meet the threshold of regulatory
significance, but do warrant advisory actions to inform the establishment of
findings that should be voluntarily corrected. Inspections classified with
VAI violations are more technical violations of the Ruminant Feed Ban. These
include provisions such as minor recordkeeping lapses and conditions
involving non-ruminant feeds.

An NAI inspection classification occurs when no objectionable conditions or
practices were found during the inspection or the significance of the
documented objectionable conditions found does not justify further actions.

The results to date are reported here both by "segment of industry" and "in
total". NOTE – A single firm can operate as more than one firm type. As a
result, the categories of the different industry segments are not mutually
exclusive.

RENDERERS

These firms are the first to handle and process (i.e., render) animal
proteins and to send these processed materials to feed mills and/or protein
blenders for use as a feed ingredient.

Number of active firms whose initial inspection has been reported to FDA –
269

Number of active firms handling materials prohibited from use in ruminant
feed – 161 (60 % of those active firms inspected)

Of the 161 active firms handling prohibited materials, their most recent
inspection revealed that:

0 firms (0.0 %) were classified as OAI

4 firms (2.5 %) were classified as VAI

LICENSED FEED MILLS

FDA licenses these feed mills to produce medicated feed products. The
license is required to manufacture and distribute feed using certain potent
drug products, usually those requiring some pre-slaughter withdrawal time.
This licensing has nothing to do with handling prohibited materials under
the feed ban regulation. A medicated feed license from FDA is not required
to handle materials prohibited under the Ruminant Feed Ban.

Number of active firms whose initial inspection has been reported to FDA –
1,074

Number of active firms handling materials prohibited from use in ruminant
feed – 444 (41 % of those active firms inspected)

Of the 444 active firms handling prohibited materials, their most recent
inspection revealed that:

0 firms (0.0 %) were classified as OAI

5 firms (1.1 %) were classified as VAI

FEED MILLS NOT LICENSED BY FDA

These feed mills are not licensed by the FDA to produce medicated feeds.

Number of active firms whose initial inspection has been reported to FDA –
5,183

Number of active firms handling materials prohibited from use in ruminant
feed – 2,391 (46 % of those active firms inspected)

Of the 2,391 active firms handling prohibited materials, their most recent
inspection revealed that:

3 firms (0.1 %) were classified as OAI

56 firms (2.3 %) were classified as VAI

PROTEIN BLENDERS

These firms blend rendered animal protein for the purpose of producing
quality feed ingredients that will be used by feed mills.

Number of active firms whose initial inspection has been reported to FDA –
386

Number of active firms handling materials prohibited from use in ruminant
feed – 183 (47% of those active firms inspected)

Of the 183 active firms handling prohibited materials, their most recent
inspection revealed that:

1 firm (0.5 %) was classified as OAI

7 firms (3.8 %) were classified as VAI

RENDERERS, FEED MILLS, AND PROTEIN BLENDERS MANUFACTURING WITH PROHIBITED
MATERIAL

This category includes only those firms that actually use prohibited
material to manufacture, process, or blend animal feed or feed ingredients.

Total number of active renderers, feed mills, and protein blenders whose
initial inspection has been reported to FDA – 6,604

Number of active renderers, feed mills, and protein blenders processing with
prohibited materials – 497 (7.5 %)

Of the 497 active renderers, feed mills, and protein blenders processing
with prohibited materials, their most recent inspection revealed that:

2 firms (0.4 %) were classified as OAI

24 firms (4.8 %) were classified as VAI

OTHER FIRMS INSPECTED

Examples of such firms include ruminant feeders, on-farm mixers, pet food
manufacturers, animal feed salvagers, distributors, retailers, and animal
feed transporters.

Number of active firms whose initial inspection has been reported to FDA –
17,227

Number of active firms handling materials prohibited from use in ruminant
feed – 5,415 (31% of those active firms inspected)

Of the 5,415 active firms handling prohibited materials, their most recent
inspection revealed that:

2 firms (0.04 %) were classified as OAI

186 firms (3.4%) were classified as VAI

TOTAL FIRMS

Note that a single firm can be reported under more than one firm category;
therefore, the summation of the individual OAI/VAI firm categories will be
more than the actual total number of OAI/VAI firms, as presented below.

Number of active firms whose initial inspection has been reported to FDA –
19,705

Number of active firms handling materials prohibited from use in ruminant
feed – 6,146 (31 % of those active firms inspected)

Of the 6,146 active firms handling prohibited materials, their most recent
inspection revealed that:

3 firms (0.05 %) were classified as OAI

200 firms (3.3 %) were classified as VAI


----------------------------------------------------------------------------
----

Issued by:
FDA, Center for Veterinary Medicine,
Communications Staff, HFV-12
7519 Standish Place, Rockville, MD 20855
Telephone: (240) 276-9300 FAX: (240) 276-9115
Internet Web Site: http://www.fda.gov/cvm


http://www.fda.gov/cvm/CVM_Updates/BSE0507.htm


10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA
2007



Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was
cross-contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI

___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL
Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal,
TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY
Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST
POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL
DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK
CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC
MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY,
A-BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not
bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007


http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html

> May 2007 Update on Feed Enforcement Activities to Limit the Spread of BSE


what about BASE ???


USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


snip...

64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD.


snip...

http://www.seac.gov.uk/minutes/95.pdf


3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western
Reserve
University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest
that BASE is more virulent than
classical BSE in humans.***


6:30 Close of Day One


http://www.healthtech.com/2007/tse/day1.asp


SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


http://www.cjdsurveillance.com/resources-casereport.html

There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf


Subject: OIE BSE RECOMMENDATION FOR USA, bought and paid for by your local
cattle dealers i.e. USDA
Date: May 14, 2007 at 9:00 am PST


http://ranchers.net/forum/viewtopic.php?p=210084#210084



IN A NUT SHELL ;

(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries.
The OIE is not responsible for inaccurate publication of country disease status based on
inaccurate information or changes in epidemiological status or other significant events that were not
promptly reported to then Central Bureau............

http://www.oie.int/eng/Session2007/RF2006.pdf


TSS
 
Why don't our cattlemen's organizations stand up against this type of practice. I wrote about this, and warned producers five years ago that we should stop these factory feedlot operations. And we claim to have the best and healthiest beef in the world, not anymore! Beef, will loose more market share from this kind of information, than from price.

Best Regards
Ben Roberts
 
Ben your comments are true to the core.

Why do our cattle organizations support such bizarre feeding practices.

Years ago, when we learned that manure was being fed to cattle, (mostly chicken manure fed to dairy cows in lower Frazer Valley, BC) we were so digusted we wrote to Health Canada. They were in the process of stopping this practice.

Mark Purdey pointed out in his papers, that chicken were fed high levels of manganese to harden the egg shell. He wrote that this could have been one source for excess bio-available manganese which was fed to cattle in the UK during the BSE crisis.

Your question, "why don't cattle organizations stand up against this type of practice?" remains unanswered by directors who are supposed to be responsible to their membership(s). They seem to answer to other individuals/organization - not you and me or the grass-route members of their cattle associations (who by the way, in Canada we pay a check-off that funds the "Alberta and Canadian Beef Producer Associations")

I have found the directors to be "unresponsive" or "condescending" when they do respond. Their priorities and motivations appears to be different from the cow/calf guys' - and to hell with what the consumer wants.

Production of beef will eventually be more "grass-fed" driven than grain.
Feedlots/ranchers are only harming themselves, by using "alternative" feeds.
 
Kathy, imagine where our industry would be now, if R-CALF, NCBA and the NFU would truly represent the producers that make up their membership. Without consumers we have nothing to market, the producers are blamed for almost everything, and we will be blamed for the feeding practices that exist today.

Why, when BSE entered Canada, didn't our cattlemens organizations on both sides of the border collectively address the issue and work on solving it. Instead of filing law suits, that damaged producers financially and they continue today, to do the same.

Best Regards
Ben Roberts
 
At the risk of being called a Hypocrite by My Northern Rancher friend - I can not help but join in on this one.

I just returned home from a meeting with a group of scientist who are going to work with us to compose a diet (with some grain) that will not destroy the CLA and good "fatty acid profile" potential in beef the way that we are destroying it now with silage and heavy grain diets. Why grain - If we all move to grass fed cattle - we will all be doomed to failure. Grass finishing is a South American specialty and they will drive us out the door on price. Grain finishing is our niche folks - but we need to find alternative supplements to stop the bleeding of CLA and good trans from our conventional feeding system.

Is this the message that the ABP folks will take back to camp? The ABP folks who had their fees paid out of the checkoff fund for the CLA conference that my wife and I attended on our own dime. I doubt it.

If we are going to make a difference Kathy and Ben, we are going to have to do it without the help of these groups. We may be able to garner support from Terry and the Bonnet gang to a certain extent. He?She has proven his/her ability to turn his/her head within the Bonnet by providing a thread that does not say BSE -- Cows BAD.

Thank you Terry dear.
 
All I can figure is the law suit is a symbol for ranchers who don't want the continued "blame" placed on their shoulders for feeding "stuff" which never should have been fed to cattle.

I don't agree with the law suit, but I do feel that there may be good which comes from it. That good is not a win for the cattleman, 'sorry'.... not directly in the lawsuit anyway; but a win in the long haul.....

The court case may bring to clearer, sharper light the fact that there is no "identifiable" infectious agent in the feed/MBM which the company is being blamed for distributing.

Joan Orr was paid over $250,000 to do a BSE risk assessment for the government of Canada. Her report concluded that you cannot measure risk for something that is not "understood". What is the so-called infectious agent?

The Canadian government didn't like her report, so they shelved it and hired a couple Brits to write the Canadian BSE risk assessment, guess who? Danny Matthews and John Collinge (I'm sure about Matthews, and only partially sure of Collinge - problems with my computer so I can't verify Collinge right now).

Danny Matthews works for VLA (Veterinary Lab Association) who did all the final testing on samples sent to UK, and he also sits on UK government committees relating to BSE and Environmental committees. He is an OIE listed expert for TSEs. He is heavily committed to the "theory" that the "infectious" prion protein is solely responsible for the disorder.

The evidence which exists surrounding the environmental findings of Mark Purdey, and the continuing developments which challenge the prion only hypothesis could potentially squash the lawsuit against Ridley.

When I have heard "rumors" of statements being made by CFIA officials, that "Purdey had it right"... I am saddened that the truth (may be) hidden from us to protect someone(s) pride.

We need to be asking ourselves what do we need to be doing to provide wholesome food and an image of wholesome food (beef).... That means limiting the amount of foreign products we introduce into our living animals, and providing fresh natural meat; no growth hormones, as few antibiotic as possible, less drugged/vaccinated cattle and stop irradiating meat for a longer shelf life.

Food gets no respect.... We can starts by trying to show our own families that eating better is the right thing to do (for a whole lot of reasons).

Ben, every year a resolution goes to the Alberta Beef Producers general meeting from the grass roots producers to "ban growth hormones" in cattle. And every year it is shot down by the delegates (usually after some big-shot tries to make anyone that supports this resolution look like a hill-billy). Last year the Board of Directors "dictated" that not all resolutions will be treated equally. Only some will go to the general meeting for voting on.... while others like the growth hormone resolution will be handled by specific committee(s).

I am disgusted! Hopefully, these actions will help some ranchers see that what the grass-roots cow calf producer wants, isn't a priority to the Big Feedlots that are encroaching more and more control upon this association. It's not just the feedlots. I have a problem with veterinarians that push the antibiotics, hormones and drug programs and ignore nutrition and environmental pollution problems. It is sad that rather than acknowledge the problems, most people would rather live and die with the symptoms and give-up.

You've heard it, I'm sure you have. "What can I do about it? I'm just one person." If nothing more, please encourage open discussion, debate and "open voting". I wear my opinions on my sleeve, most of the time. I wish more people would openly discuss their own opinions. I can't tell you how many times someone else's opinion/evidence to support it... has changed my view of things. People should not be shy or embarassed. In the long run, we will make a difference if we just share our voices.
 
Kathy said:
snip...

Joan Orr was paid over $250,000 to do a BSE risk assessment for the government of Canada. Her report concluded that you cannot measure risk for something that is not "understood". What is the so-called infectious agent?


GLAD you ask kathy, here is the answer to your question. you should file these away, so you can go back and go over them when you forget :wink:



WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;


Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa

It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


2

6. It also appears to me that Mr Bradley's answer (that it would take less than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise that it

could take as little of 1 gram of brain to cause BSE by the oral route within the

same species. This information did not become available until the "attack rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to ensure

that the actual result was within both a lower and an upper limit within the study

and the designing scientists would not have expected all the dose levels to trigger

infection. The dose ranges chosen by the most informed scientists at that time

ranged from 1 gram to three times one hundred grams. It is clear that the designing

scientists must have also shared Mr Bradley's surprise at the results because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]

http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm


2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml




12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON
SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY snip... A The Present
Position with respect to Scrapie A] The Problem Scrapie is a natural disease
of sheep and goats. It is a slow and inexorably progressive degenerative
disorder of the nervous system and it ia fatal. It is enzootic in the United
Kingdom but not in all countries. The field problem has been reviewed by a
MAFF working group (ARC 35/77). It is difficult to assess the incidence in
Britain for a variety of reasons but the disease causes serious financial
loss; it is estimated that it cost Swaledale breeders alone $l.7 M during
the five years 1971-1975. A further inestimable loss arises from the closure
of certain export markets, in particular those of the United States, to
British sheep.


9/13/2005
----------------------------------------------------------------------------
----
Page 17
Page 17 of 17


It is clear that scrapie in sheep is important commercially and for that
reason alone effective measures to control it should be devised as quickly
as possible. Recently the question has again been brought up as to whether
scrapie is transmissible to man. This has followed reports that the disease
has been transmitted to primates. One particularly lurid speculation
(Gajdusek 1977) conjectures that the agents of scrapie, kuru,
Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are
varieties of a single "virus". The U.S. Department of Agriculture concluded
that it could "no longer justify or permit scrapie-blood line and
scrapie-exposed sheep and goats to be processed for human or animal food at
slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the
finding that some strains of scrapie produce lesions identical to the once
which characterise the human dementias" Whether true or not. the hypothesis
that these agents might be transmissible to man raises two considerations.
First, the safety of laboratory personnel requires prompt attention. Second,
action such as the "scorched meat" policy of USDA makes the solution of the
acrapie problem urgent if the sheep industry is not to suffer grievously.


snip...


76/10.12/4.6



http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf



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.

PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract



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.

PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract



1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8



Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

PMID: 8006664 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract


tss
 

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