Thursday, May 1, 2008

Cargill, National Beef Packing Engaged in Inhumane Practices

Cargill, National Beef Packing Engaged in Inhumane Practices

Date Published: Thursday, May 1st, 2008

In the wake of this year’s Hallmark/Westland meat recall, representing the largest such recall in US history, the Associated Press (AP) is reporting that two of this country’s largest meat processors, “were slapped with humane handling violations.” The violations were discovered during a governmental review as part of the National School Lunch Program.

Earlier this year, Hallmark/Westland Meat Packing Company recalled 143 million pounds after plant workers were caught on videotape forcing unfit cattle into slaughter. At least 37 million pounds of that meat was used for school lunches and federal nutrition programs, according to the USDA. The recall came three weeks after the Humane Society of the US released videotapes from an undercover investigation exposing Hallmark/Westland workers abusing sick and injured cattle. Meat from “downer” cattle—animals too ill or injured to walk—is not generally released into the food supply to help prevent against the deadly, brain-wasting “mad cow” disease. The Hallmark/Westland cattle were unable to stand at the time of slaughter, although they passed inspection earlier. When this occurs, packers are required to alert USDA veterinarians so they can decide if the animal can be slaughtered for food.

Meanwhile, recent audits conducted by the Agriculture Department’s Food Safety and Inspection Service (FSIS) and prompted by the Hallmark/Westland recall, found National Beef Packing Company plant in Dodge City, Kansas and a Cargill Meat Solutions plant in Fresno, California to be in “noncompliance.” Also, 18 slaughterhouse audits revealed cattle were not always initially properly stunned, some were overcrowded, and others required electric prodding. One violation was so serious that it led to a temporary suspension.

The FSIS temporarily shut down Martin’s Abattoir and Wholesale Meats in Godwin, North Carolina, for “insufficiently stunning animals” and “failing to make them insensible to pain on the first attempt.” The FSIS also issued a noncompliance order to Dakota Premium Foods—South St. Paul, Minnesota—for “excessive bunching up of cattle going into the stunning area.” The FSIS also cited National Beef for “overcrowded holding pens.”

FSIS officials said that in reviewing 36 animals at Cargill, virtually all refused to enter the restraint; an electric prod had to be used on 10. Three still refused and required stunning and being rendered unconscious “so that they could be pulled through the restrainer to be shackled, hung and bled,” the noncompliance record states. Cargill spokesman Mark Klein said the prods did not have batteries, so there was no electric current and that it was the audit process that caused the problems. “We believe the reason for the animals balking, or not moving forward,” he said, “was that there were too many people present during the audit, distracting the animals,” citing two or three additional government people and three or four additional Cargill employees.

The FSIS disagreed saying, “That’s just not the case,” said Eamich, the FSIS spokeswoman. “Our auditors are trained, they know how to conduct audits, to allow business to go on as usual, just as if some of our inspectors were there. It’s really no different.”

This entry was posted on Thursday, May 1st, 2008 at 8:45 am and is filed under Legal News, Food Poisoning.

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Terry S. Singeltary Sr. Says:

May 1st, 2008 at 9:38 am


Subject: [madcow] Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46 Friday, April 25, 2008


MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE

Tuesday, April 29, 2008

Interference at the EPA - Science and Politics at the U.S. Environmental Protection Agency

please see full text ;

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

Creutzfeldt-Jakob Disease (Variant) and Bovine Spongiform Encephalopathy (Prion Diseases) Description Since 1996, strong evidence has accumulated for a causal relationship between ongoing outbreaks, primarily in Europe, of a disease in cattle called bovine spongiform encephalopathy (BSE, or “mad cow disease”) and a disease in humans called variant Creutzfeldt-Jakob disease (vCJD). Both disorders, which are caused by an unconventional transmissible agent, are invariably fatal brain diseases with incubation periods typically measured in years (1). Transmission of the BSE agent to humans, leading to vCJD, is believed to occur via ingestion of cattle products contaminated with the BSE agent; the specific foods associated with this transmission are unknown. However, a recently published case-control study involving 132 vCJD cases in the United Kingdom (UK) showed evidence of an increased risk for vCJD associated with the frequency of consuming beef products likely to contain mechanically recovered meat and head meat (such as burgers, meat pies, and sausages) (2). Bioassays and molecular tests have enabled identification of what World Health Organization consultants have classified as “high-infectivity” and “lower infectivity” tissues of cattle with BSE (3). The high-infectivity tissues include the brain, spinal cord, retina, optic nerve, and dorsal root and trigeminal ganglia, suggesting that these tissues can pose a relatively high risk of transmission. The lower infectivity tissues include peripheral nerves (e.g., sciatic and facial nerves), tonsils, nictitating membrane (third eye lid), distal ileum, bone marrow, and possibly thigh muscle. The latter tissue from one cow with BSE transmitted disease to highly BSE-sensitive transgenic mice at a rate indicative of trace levels of infectivity.

Thursday, April 24, 2008



Sunday, April 20, 2008

Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008

who’s gonna be following these children over the next decade or so to see if they contract CJD ? the USDA? FSIS? FDA? CDC? NIH? we must not forget, these innocent children were exposed to the most high risk ‘banned’ animals for BSE/TSE mad cow disease. the other firewall they were speaking of protecting these children would have been the feed ban, which we now know was nothing more than ink on paper. 3 suspect CJD cases as we speak in females under 30 in the USA, other young victims in the USA with CJD. who’s going to follow the children from this nationwide long term case study of children to the TSE agent via the most high risk animals i.e. dead stock downer cattle i.e.. non-ambulatory ???

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 England.


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.


UK today ;

My son died of CJD – now I want answers

A mother has told how her son was left unable to feed himself or even speak by the rare variant Creutzfeldt-Jakob disease. Andy Black died five months after being diagnosed with the killer brain bug – the human strain of mad cow disease.

During that time his mum Christine Lord was forced to watch helplessly as the 24-year-old’s condition deteriorated.

She kept a vigil at her son’s bedside as she was forced to watch him die, holding him for four days after his brain died before he finally passed away at the family’s Southsea home on December 16.

Now Christine, who is a journalist, has vowed to get justice for Andy and more than 200 people who have died from the disease in the UK.

She said: ‘The memories of my son, the way he died and the fact it was avoidable will stay with me for the rest of my life.

‘I was by Andy’s side through all of this. For every procedure he went through I was holding his hand.

‘People need to know there are people who are still in charge of this country who have allowed lives to be destroyed by CJD.’

It is believed Andy contracted CJD before 1994, but it can take years to develop. His symptoms started to show at the end of 2006 when he became tired and withdrawn.

However he was not diagnosed with the disease until July last year. Christine never told Andy he had the disease. From then, his condition deteriorated rapidly.

She said: ‘They told me in a little room and then I had to go back in and say everything was all right.

‘How can you tell at 24-year-old man he’s dying from CJD?

‘I had to cope with it. I’m his mum. I had to give Andy hope, even if it was just for a day.’

Christine Lord’s quest for justice will be aired on BBC1’s Inside Out programme at 7.30pm tomorrow.



THESE cases that have come about recently in the very young are most disturbing.

a 22 year old last week died, she is suspect nvCJD. never left US. PORTSMOUTH, Va. — A 22-year-old Portsmouth woman is close to dying, and family says doctors believe the human equivalent of Mad Cow Disease could be the reason.

another young female suspect nvCJD that is 26 years old in Alabama, She is in the final stages of CJD. She is at home in a hospital bed…very skinny…and at times in the past month has had some eating and swallowing issues. Sometimes she rallies and starts eating again. She stopped walking at Christmas. they do not expect her to live much longer than May, since that would be 14 months since her first major symptom of CJD (personal communication).

AND now, a 3rd young female, 23 years old. hmmm, i am pondering about just how long all those downers were in the school lunch program, and IS the incubation period catching up now ??? is this the first of many more to come ???

Family fighting for answers about daughter’s disease

Reported by: Kristen Cosby Email: Last Update: 4/18 9:57 pm

JACKSONVILLE, Fla. — A family is fighting for answers about their dying daughter.

Her family says doctors tell them 23 year old Rachel Woodard has a rare brain disease that could be the human form of mad cow. She’s been hospitalized for five months after she started having severe seizures.

“I’m scared to death I’m going to lose my daughter,” said her dad Norman Woodard.

Rachel’s family says doctors have told them she has Creutzfeldt-Jakob Disease… or CJD.

“He said he was 99 percent positive that’s what it is,” said Rachel’s Aunt Loretta Mallard.

CJD can come from eating an animal diseased with mad cow. It can also hit people completely by random.

“There is no treatment for cjd. its by definition a universally fatal disease,” said epidemiologist Roger Sanderson.

CBS47 can’t confirm in Rachel has CJD. Privacy laws prevent her doctors from talking about her health, but CJD can only truly be confirmed by a brain autopsy.

The family says doctors are doubting their original diagnosis. Rachel’s dad wants a second opinion, but he doesn’t have the power of surrogacy. Rachel gave that to her boyfriend.

“I’m more scared of the hospitals misdiagnoses more than anything else. i’m scared she’s going to die of a misdiagnoses,” said Woodard.

Rachel’s boyfriend, who has power attorney, wants to protect what is left of Rachel’s privacy. He says after numerous attempts by medical experts, Rachel ’s family has failed to accept or understand the true diagnosis. In response to her family’s request of a second opinion, he says Shands was her second opinion because she was previously admitted back in December.

NOW, what are we missing, besides our minds ???

re-Association between Deposition of Beta-Amyloid and Pathological Prion Protein in Sporadic Creutzfeldt-Jakob Disease


Thursday, May 1, 2008

DEAD STOCK DOWNER COW BAN i.e. non-ambulatory policy still not changed by USDA May 1, 2008

Sunday, May 17, 2009


Sunday, September 6, 2009






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