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From: TSS ()
Subject: US May Need Animal-Health Czar to Protect Consumer
Date: July 19, 2005 at 8:31 am PST

US May Need Animal-Health Czar to Protect Consumer


USA: July 19, 2005

WASHINGTON - Consolidating US animal disease oversight under one high-level government czar may be the best way to protect consumers from mad cow disease, bird flu and other serious animal ailments that can jump species, a National Academy of Sciences panel said on Monday.

The Academy's National Research Council, which advises the US government on scientific and environmental matters, criticized the current animal health system as too convoluted at a time when new diseases are emerging and experts worry about bioterrorism targeted at the food supply.
More than 200 different US government offices, seven Cabinet-level departments and hundreds of state and local agencies share in the responsibility of regulating animal health.

"To strengthen the existing framework, the nation should establish a high-level, authoritative mechanism to coordinate interactions between the private sector and local, state and federal agencies," the panel said.

The agriculture secretary has been the main point-person for recent US outbreaks of mad cow disease, chronic wasting disease and a less-virulent strain of avian influenza. Almost three-quarters of animal diseases can infect humans, according to the National Research Council panel led by Lonnie King, dean of veterinary medicine at Michigan State University.

Humans can contract a form of mad cow disease, or bovine spongiform encephalopathy, by eating infected meat.

The H5N1 strain of bird flu in chickens and ducks has been linked to more than 50 human deaths in Asia since 2003. The World Health Organization has warned that bird flu could kill millions of people if it mutates and acquires the ability to pass easily from human to human.

The committee of independent scientists stopped short of recommending that the Bush administration create a new senior job for overseeing animal diseases, saying it has not yet completed its evaluation of the US animal health system.

The government could also centralize authority by creating an interagency alliance or a domestic version of the Paris-based World Organization for Animal Health (OIE), it said.


The scientists also said they found "significant delays" in developing and adopting new technologies that would help detect serious animal diseases.

The panel supports a more comprehensive livestock identification system and research to develop a "live animal" test for preventing mad cow disease.

Last month, the USDA revised its testing program on the brains of slaughtered cattle to include a more sophisticated test already in use in Europe and Asia.

The administration took the action after acknowledging it had misdiagnosed a "downer" Texas beef cow using its testing protocol in November. The animal tested positive for the disease last month using the more sophisticated test.

"This case raises questions about the type and accuracy of diagnostic tests used by USDA," the committee said. It did not elaborate.

The committee also raised concerns about the steady decline of veterinarians in federal and state agencies. "The work force on the frontlines of animal care is not adequately educated and trained to deal with animal disease issues," it said.

The USDA predicts a shortfall of several hundred veterinarians on its staff by 2007, as more professionals are attracted to caring for pets and companion animals rather than livestock, the 237-page report said.

Story by Randy Fabi


Gerald Wells: Report of the Visit to USA, April-May 1989


The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...


It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...


3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...


To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

•Department of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in


Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough
and Burger who demonstrated that the disease was transmissible with a long incubation
period, and that affected mink had a spongiform encephalopathy similar to that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965).
Because of the similarity between TME and scrapie, and the subsequent finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was
concluded that TME most likely resulted from feeding mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time provided
evidence that they may be different. Epidemiologic studies on previous incidences of
TME indicated that the incubation periods in field cases were between six months and
one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be
transmitted to mink in less than one year.
To investigate the possibility that TME may be caused by a (particular strain of
scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie
agent, including their sheep or goat sources, were inoculated into a total of 61 mink.
Only one mink developed a progressive neurologic disease after an incubation period of
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused
by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent
from an unidentified source.


A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were "acting funny", and some had died. At this time, we
visited the farm and found that approximately 10% of all adult mink were showing
typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over
their _backs like squirrels. These signs were followed by progressive deterioration of
neurologic function beginning with locomoior incoordination, long periods of somnolence
in which the affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over the past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy
cattle and a few horses. Sheep had never been fed.

Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after incubation
periods of four months. To investigate the possible involvement of cattle in this disease
cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally
with a brain suspension from affected mink. Each developed a fatal spongiform
encephalopathy after incubation periods of 18 and 19 months.

These findings suggest that TME may result from feeding mink infected cattle and
we have alerted bovine practitioners that there may exist an as yet unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new
bovine spongiform encephalopathy has recently been reported in England (Wells et al.,
1987), and investigators are presently studying its transmissibility and possible
relationship to scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be
confused with rabies in the United Stales and not be diagnosed. Presently, brains from
cattle in the United States which are suspected of rabies infection are only tested with
anti-rabies virus antibody and are not examined histopathologically for lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no agent-
specific proteins or nucleic acids identified for these transmissible neuropathogens, one
means of distinguishing them is by animal passage and selection of the biotype which
grows best in a particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral
backpassage of the experimental bovine agent resulted in incubations of only four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine passage.
Mink fed infected bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.

These studies were supported by the College of Agricultural and Life Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United
States Department of Agriculture. The authors also wish to acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.

Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.


Subject: Mad cow blamed on CFIA ''Canada followed U.S. policies''
Date: July 13, 2005 at 12:51 pm PST

Agency blamed for mad cow fallout


OTTAWA (CP) - Canada's $8-billion mad cow disaster can be squarely attributed the failure of the Canadian Food Inspection Agency to assess economic consequences of even a single infection, says a leading expert.

William Leiss of the University of Ottawa, who is also a past president of the Royal Society of Canada, said the CFIA assessed the risk of mad cow to animal health and human health, but not the risk of losing export markets. Yet Canada was party to an international agreement providing for a ban on exports from any country with even a single case of the disease. The policy was known as "one cow and you're out."

"What would be the economic impact of one or just a few cases of BSE (bovine spongiform encepalopathy) in the Canadian herd?" Leiss asked at a World Health Organization conference on risk management.

"We failed completely to manage or even to recognize this risk at our great cost."

He said Canada followed U.S. policies in adopting a minimal testing program. But Canada's risk profile is completely different from that of the United States.

At the time, Canada exported 75 per cent of beef production while the United States exported only 10 per cent. Losing export markets was not a serious problem for the Americans, he said.

"In food issues we are cursed with the political attitude that we've just got to be onside with the U.S. and nothing else matters."

He said the CFIA also followed the U.S. lead in making a half-hearted effort to stop recycling infected protein in ruminant food, which is widely believed to be the cause of mad cow disease.

Leiss said the CFIA ban on feeding proteins from ruminants to ruminants remains "full of holes."

Leiss said the United States conducted a full risk assessment in 1997-98, but Canada did not do one until six years later.

CFIA spokesman Marc Richard said the agency didn't include economic consequences in its assessment because that is not the agency's mandate.

"We don't usually address the economic stuff," said Richard in an interview. "The risk assessment was based strictly on the disease. Overall we're the administrators of the Animal Health Act.

"The CFIA's risk assessments have to do with animal disease. That is our mandate and in our mandate we specifically don't address economics."

But another CFIA official, senior veterinarian Darcy Undseth, said economic consequences of a mad cow infection in Canada were considered in a 2002 risk assessment even though they were not quantified.

He said the consequences were described in that assessment as "extreme."

Undseth said the CFIA's response was "very successful because of the proactive steps taken since 1990 and the very measured response taken in a North American context.

"BSE has not established and amplified in North America but was captured on its way to eradication."

Asked about the estimated $8 billion in economic losses to date, Undseth said animal diseases do have economic impact but the BSE response "has been a successful program."


Working Group Report on the Assessment of the Geographical BSE-Risk (GBR
III) of USA 2004 ''extremely/very unstable BSE/cattle system''




Canada and the United States have been raised to level III (presence of BSE likely but not confirmed, or confirmed at a lower level) following a new assessment taking into account the most recent evidence. EFSAs Scientific Expert Working Group on geographic BSE risk assessment also evaluated the status of Mexico and South Africa which were classified as level III.

From: Terry S. Singeltary Sr. []
Sent: Tuesday, July 29, 2003 1:03 PM
Cc:;; BSE-L
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

Greetings FDA,


PLUS, if the USA continues to flagrantly ignore the _documented_ science to date about the known TSEs in the USA (let alone the undocumented TSEs in cattle), it is my opinion, every other Country that is dealing with BSE/TSE should boycott the USA and demand that the SSC reclassify the USA BSE GBR II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the SSC to _flounder_ any longer on this issue, should also be regarded with great suspicion as well. NOT to leave out the OIE and it's terribly flawed system of disease surveillance. the OIE should make a move on CWD in the USA, and make a risk assessment on this as a threat to human health. the OIE should also change the mathematical formula for testing of disease. this (in my opinion and others) is terribly flawed as well. to think that a sample survey of 400 or so cattle in a population of 100 million, to think this will find anything, especially after seeing how many TSE tests it took Italy and other Countries to find 1 case of BSE (1 million rapid TSE test in less than 2 years, to find 102 BSE cases), should be proof enough to make drastic changes of this system. the OIE criteria for BSE Country classification and it's interpretation is very problematic. a text that is suppose to give guidelines, but is not understandable, cannot be considered satisfactory. the OIE told me 2 years ago that they were concerned with CWD, but said any changes might take years. well, two years have come and gone, and no change in relations with CWD as a human health risk. if we wait for politics and science to finally make this connection, we very well may die before any decisions
or changes are made. this is not acceptable. we must take the politics and the industry out of any final decisions of the Scientific community. this has been the problem from day one with this environmental man made death sentence. some of you may think i am exaggerating, but you only have to see it once, you only have to watch a loved one die from this one time, and you will never forget, OR forgive...yes, i am still very angry... but the transmission studies DO NOT lie, only the politicians and the industry do... and they are still lying to this day...TSS

Terry S. Singeltary Sr. P.O. BOX 42 Bacliff, TEXAS USA

From: TSS ()
Date: July 5, 2005 at 8:46 am PST

Department of Health and Human Services Public Health Service
Food and Drug Administration

Minneapolis District Office
Central Region
212 Third Avenue South
Minneapolis, MN 55401
Telephone: (612) 758-7119
FAX: (612) 334-4142

June 9, 2005



Refer to MIN 05-15

Michael J. Langenhorst
Anamax Corporation
P.O. Box 10067
Green Bay, WI 54307

Dear Mr. Langenhorst:

Our inspection of your rendering plant located at 505 Hardman Avenue South, South St. Paul, Minnesota, from January 12-20, 2005, revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations , Part 589 .2000 (21 CFR 589 .2000), Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). Because you failed to follow the requirements of this regulation, products being manufactured and distributed by your facility are adulterated within the meaning of Section 402(a)(4) of the Federal Food, Drug, and Cosmetic Act (the Act) [21 U.S.C. 342(a)(4)], and misbranded within the meaning of Section 403(a)(1) of the Act [21 U.S.C. 343(a)(1)].

Our investigation found that you failed to provide for measures to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] in that:

1. You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into feeds that may be used for ruminants.

2. You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds that may be used for ruminants.

Our investigation also found that you failed to label products that may contain protein derived from mammalian tissues with the statement, "Do not feed to cattle or other ruminants." For example, your Feather Meal and Stabilized Poultry By-Product Meal lack this statement, even though the absence of sufficient measures to avoid commingling or cross-contamination may result in these products containing protein derived from mammalian tissues. Because your products do not bear this caution statement, they are misbranded under Section 403(a)(1) of the Act [21 U.S .C. 343(a)(1)).

The above is not intended as an all-inclusive list of violations. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring that your overall operation and the products you manufacture and distribute are in compliance with the law.

You should acknowledge this letter within 15 working days of receiving and include any additional corrective actions concerning your facility. We have received your letter dated January 31, 2005, which replies to the Form FDA-483 issued on January 20, 2005, and your letter dated February 25, 2005, that states all corrections have been implemented. The corrections you have reported appear to be adequate but will be evaluated further during our follow-up inspection.

Your response should be directed to Compliance Officer Jane E . Nelson at the address on the letterhead. If you have any questions regarding this letter, you may phone Ms. Nelson at (612) 758-7119.



W. Charles Becoat
Minneapolis District

ntification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)Docket No, 04-047-l Regulatory Ide


Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in

Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed

Comment Number: EC -10

Accepted - Volume 2



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