Mad Cow Home ... Best Links ... Search this site

Cattlemen lose Texas veggie libel case.
They knew all along
Spoof of trial: 'The Ballad of Oprah and Howard': off-site US experience with experimental bovine TSE
The Stetsonville mink: was it bovine TSE?
Downer cow prevention
Economist: Don't Blame Oprah
Cutting greenhouse gas emissions from cattle
Europe could face 'devastating' outbreaks of animal diseases
Cattle disease release threatened in NY subways
Restaurant owner faces jail for serving T-bone steaks

Judge Tosses Part of Winfrey Case

AP 18 Feb 98 By Mark Babineck

The judge dismissed the hamburger disparagement portion of the lawsuit brought by the Texas feedlot operator against Oprah Winfrey and Howard Lyman of the Humane Society. An even more far-fetched common-law business disparagement case is left which places even greater burdens on the plaintiff.

The dismissal was done in such a way as to essentially prevent any appeals by the cattle industry: the judge simply threw out the case without giving reasons. There is nothing to hang your hat on in an appeal. The defense had not even begun its case.

The cattlemen picked a state with one of the weakest food disparagement laws, an event with non-existent factual errors, a law trumped in any event by the First Amendment, sued the most popular and trusted woman in America, thus hugely promoting national awareness of an issue that otherwise would have been quickly blown off as talk show talk. Dumb. -- webmaster opinion

The first test of the nation's 13 ``veggie libel'' laws has come back with an incomplete grade. The federal judge in Oprah Winfrey's beef defamation trial on Tuesday tossed out part of the case filed under Texas' food defamation law. But Judge Mary Lou Robinson, without explanation, rejected a defense request to throw the case out entirely.

Jurors were to return today to hear the lawsuit as a common-law business disparagement case, which has a heavier burden of proof on the plaintiffs. Cattlemen blame Ms. Winfrey's April 16, 1996, talk show about dangerous foods -- it included a segment on mad cow disease -- for causing cattle prices to plummet. They say the program cost them $12 million.

The case is the first court test of any of the ``veggie libel'' state laws and some experts had predicted it could become the Supreme Court test. Robinson's ruling eliminated that possibility. She did not declare the Texas law unconstitutional; she instead ruled the cattlemen had failed to make a case under the law during the four weeks of the trial.

States passed ``veggie libel'' laws after Washington state apple growers unsuccessfully sued CBS over a 1989 ``60 Minutes'' segment about the potential dangers of a fruit coating called Alar. Without a specific food disparagement law at the time, apple producers sued under disparagement laws. The cattlemen find themselves in the same situation.

``It appeared to me (cattlemen) were stressing the `veggie libel' claims,'' said Bruce Johnson, the attorney who defended CBS. ``They were putting all their eggs in the `veggie libel' basket, and the judge's decision apparently cuts the heart out of their case.''
Cattlemen now must show Ms. Winfrey, her production company and a vegetarian activist guest on the show meant to damage the beef industry.

Under the ``veggie libel'' law, they only had to prove that knowingly false statements were made. Attorneys refused to discuss the ruling, citing a gag order. Defense attorneys have argued that livestock aren't perishable food, and that the cattlemen's theory would allow any person who owned a cow to have cause for legal action.

In a motion filed Tuesday morning, cattlemen said they believe there's been enough evidence presented to support the disparagement case. The cattlemen say Ms. Winfrey and activist Howard Lyman gave the impression on her show that U.S. cattle were at risk for mad cow disease, found in English livestock and suspected in 23 deaths in Britain. Mad cow disease and its human counterpart never have been detected in the United States.

Beef Group Knew Oprah Show Lineup

The Associated Press By MARK BABINECK 22 Feb 98
AMARILLO, Texas - A spokeswoman for a beef industry trade association testified Monday that far from being ambushed, the group knew it would be up against an anti-meat crusader on ``The Oprah Winfrey Show.''

Alisa Harrison, a spokeswoman for the National Cattlemen's Beef Association, said she approved of allowing specialist Gary Weber to debate vegetarian activist Howard Lyman over whether mad cow disease threatened U.S. cattle.

``We can take Howard Lyman,'' Ms. Harrison wrote in notes that were entered as evidence. ``Confidence in beef is high and we can keep it there. Our members watch Oprah, and if we're not there, they'll want to know why.''

A group of Texas cattlemen is suing Ms. Winfrey, her production company and Lyman for $12 million, saying the April 16, 1996, episode falsely implied mad cow disease threatened U.S. cattle and caused cattle prices to plummet. Ms. Harrison took the stand as a witness for Ms. Winfrey.

Weber has testified that the way his comments were edited in the show's final version was unfair. Ms. Winfrey has told jurors that some of Weber's comments were taken out because they were imprecise. She denied that he was ``ambushed.''

After the NCBA complained of being ``duped,'' Ms. Winfrey invited Weber back on the show a week later to make his points one-on-one.

National Cattlemens Beef Association president John Lacey, in letters cited by the defense, applauded Ms. Winfrey for showing ``an honest commitment to fairness.''

A few days later, Lacey also wrote that cattle producers were suffering the ``worst cost-price squeeze ... since the 1970s'' because of drought, high feed costs and cheap competing meats. He made no mention of Ms. Winfrey's show.

Scrapie US bovines reviewed

Wed, 18 Feb 1998 webmaster
A recent article in the J Comp Pathol 1997 Oct;117(3):271-275 addresses a continuation of the successful Mission, Texas transmission of sheep and goat TSE to US cattle. See also RC Cutlip et al. J. Inf. Dis 169 814 1994 and WW Clark et al. Am J Vet Res 56#5 606 1995

These are not easy experiments to do because at ARS Ames, AALACI humane standards of care for the animals are met, as well as agricultural biosecurity level II containment.

US scrapie was imported to Michigan from the UK in Suffolk sheep; the first outbreak was in 1947. There were further imports of scrapie Suffolk to Canada which surfaced in 1952-53 in Illinois, California, and Ohio. I don't believe these have a known strain type within the English nomenclature system or whether the strain types are the same. The genotype was never determined at any time.

The US scrapie eradication program was dismantled in 1983 deregulation under Reagan (the US Thatcher) so only lamb and mother, female line within flock were slaughtered, source flock ignored, causing disease incidence to soar and become established and widespread across 39 states according to Hadlow, JAVMA 196 1676 1990. It is hard to know what is going on with US scrapie incidence today due to lack of meaningful reporting standards. There is less of problem in goats though cross-species lateral transmission in mixed flocks seems an unavoidable inference (with relevence to CWD?).

Given the US rendering situation and problems with goats, but prior to developments with BSE in the UK and Stetsonville, the question came up in 1979, could scrapie pass to cows (bovine scrapie) and what is the extent of this disease in the US?

Cattle were successfully inoculated in 1979 in a Mission, Texas APHIS facility both from scrapie passaged in a Suffolk ewe from a pool of 4 scrapie sheep and separately from a passage of goat to goat (co-pastured with same sheep, caprine scrapie). WW Clark et al. Am J Vet Res 56#5 606 1995.

The good news in the Cutlip et al. 1997 paper reviewed here, the cow-to-cow second passage study, is that while the pooled US forms of scrapie considered do indeed induce a transmissible prion disease passagable with consistent symptoms and incubation times in cattle, that disease is clearly not the UK strain of bovine TSE even at second passage when sheep prion protein is long gone. Not particularly spongiform, so technically a TE or BE rather than TSE or BSE. The pathological documentation for this in the paper is excellent.

The bad news is that:

(1) US scrapie easily crosses the species barrier to cattle (and goats). Some other unstudied US strain of scrapie could cause the BSE strain of bovine TSE. The results here clearly disfavor the idea that UK BSE came from sheep, but do not disprove it. The origin of UK BSE remains unknown (as does the much older origin of scrapie). Neither cattle nor sheep prion genotypes nor strain types were determined here.

(2) The prevalence in non-experimental US cattle populations of the Mission, Texas experimental sheep-to-cow type TE remains unknown. We do know that scrapie is common, widespread, and for all practical purposes, uncontrolled, and that sheep carcasses are not wasted.

The USDA monitoring program is largely moot: it is geared towards detecting British BSE, not Texas scrapie-BSE and related strains.

These US bovine scrapie animals have a very different clinical presentation and a very different histology from UK BSE. Recumbancy is described as the dominant symptom. The main thing noticed on both passages is lethargy, stiffness, and ataxia, leading to recumbancy, with animals lying down and have increasing difficulty getting up.

Clark et al write, "At no time did the cattle appear apprehensive, aggressive or unduly excitable. Their responses to sound and touch were not exaggerated and their vision seemed unimpaired. None had pruritus. When down on it side, each animal sometimes paddled but never thrashed about or had convulsions, now were whole-body convulsions observed. All cattle continued to eat and were in good physical condition at euthasia."

JL Hourigan in JAVMA 196 #10 1678 1990, described scrapie-affected cattle as "downers" with "running in place" [his quotes] which is apparently a slaughterhouse term for recumbent paddling and a recognized subset of overall 'downer' cattle.

(3) These are not the symptoms of scrapie in the sheep used for inoculation. It seems that a marked change in agent behavior has occured with trans-species passage. The histology would be unrecognized as a TSE were it not for prion immuno-assay, passaging transmission, and inoculation history.

(4) The USDA regretably focused on British BSE and rabid cows from Kentucky when they could have emphasized prion immuno-assays (not UK BSE patholology training) on "downers" with "running in place." How many of this critical subset of 'downer' cows are in the 6,000 brains studied? Obviously, the USDA would be well aware of all the papers cited here. I think that they have done the cattle and pharmaceutical industries a real disservice with an ineffectual program.

(5) Transmissibility to humans of the Texas scrapie-BSE strain and other US scrapie-BSEs remains unknown. There is no reason why the result should resemble nvCJD or even be diagnosed as any CJD. It would be good to do transmission to transgenic mice and in vitro conversion studies: a lethal, transmissible US BSE wouldn't be much of an improvement over UK BSE.

US scrapie-BSEs could be better, same, or worse for humans than British BSE. The transmissibility of sheep scrapie to humans is moot: we are talking cow prion sequences and strains now and bovine TSE, not sheep prions and scrapie.

(6) Note that the cow-to-mink-to-cow bovine TSE studied by Marsh is quite different from the Texas scrapie-BSE strain: affected animal behavior is different and the spongiform aspect is pronounced. I don't know if the Wisconsin BSE has been conclusively differentiated from UK bovine TSE; the US imported some MBM but the onset in Wisconsin is very early. The Texas, Wisconsin, and British cows show that bovine TSE presents in widely variant forms according to strain type (just like scrapie, CJD, TME and murine TSE).

A couple paragraphs from the Stetsonville, Wisconsin mink outbreak of 1985. Some people read the article as saying scrapie caused mink TSE. This would involve the mink farmer mistaking a sheep for a horse or cow as he personally rendered them, not real plausible:

"This mink farmer used no commercially available animal by-products in his feed, but instead slaughtered all animals going into the mink diet, which included mostly (over 95%) "downer" dairy cows, a few horses but never sheep. To examine the possibility that cattle may have been the source of this incident of TME, two 6-week-old Holstein bull calves were inoculated intracerebrally with mink brain from the affected farm. The bulls developed neurologic disease 18 and 19 months after inoculation. Both brains had spongiform degeration at necropsy and both were transmissible back to mink by either intracerebral (incubation period of 4 months) or oral (incubation periold of 7 months )inoculation. Whereas TME has been thought to be caused by feeding scrapie-infected sheep to mink, this theory has no conclusive evidence. Experimental oral inoculation of mink with several diffferent sources of sheep scrapie has never been successful, and an incubation period of less than 12 months has never [been] produced in intracerebral inoculation."
Bovine spongiform encephalopathy in the United States
RF Marsh JAVMA 196: 1677 1990

(7) If the goal is to truly protect the human food and drug supply in the US plus safety of exports to the EU, then we need to treat all bovine TSEs, indeed all TSEs, on the same risk footing as UK BSE until proven otherwise. The report reviewed here definitely ups the ante.

The Stetsonville mink: was it bovine TSE?

22 Feb 98 listserve and webmaster opinion
Very interesting posts about sheep industry realities. Indeed reported scrapie, like reported BSE, is very much influenced by the regulatory and economic climate. I believe the evidence supports your opinion that 'the mink story is more plausible evidence for cattle S.E.s in the U.S.' than scrapie or scrapie-in-cattle [see below]' However:

(1) Reported scrapie incidence, which in the final analysis is the only historical data we have, did indeed triple after the Scrapie Eradication Program ended. For 1984-88, outbreaks averaged 37 per year and 52 flocks in 20 states from October 1988 to June 1989.

Scrapie had been _reported_ in 460 flocks in 39 states by 1990. As always, the issues are reporting extent and pre-clinical carriers. Ten breeds of sheep have been affected, including Ramboillet and Targhee. As you say, most have been flocks of Suffolk. Hampshire and Cheviot most often after that. And most of the non-Suffolk and all of the goats were traceable to contact with infected Suffolk. JAVMA 196 1676 90.

(2) I don't fully agree that "when BSE first became known, rendering plants stopped accepting dead sheep." This was a gradual process that continued at least up to mid-1997 for sheep rendering facilities such as one in western Canada. UK BSE 'became known' on 22 Dec 1984 in Midhurst, West Sussex, UK and if you interpret Stetsonville, Wisconsin as a US strain of bovine TSE, that dates to April, 1985. In what year did Dixon start sending sheep to the Kettelman hazardous landfill?

The cattle in this particular sheep-to-cattle experiment received a quadruple inoculum "to increase the liklihood of infection:" 5 ml in muscles of shoulder, 5 ml under skin behind elbow, 1 ml in parietal cerebrum, and 30 ml by mouth. WW Clark et al. Am J Vet Res 56#5 606 1995 or JAVMA 196 1678 1990.

Prior to Reagan getting the Scrapie Eradication Program of 1952 off the backs of the woolgrowers [perhaps at their own request], there had been the initial 1947 Michigan outbreak, several flocks in 1952 and 1953, then 10-14 flocks per year through 1968, then reported outbreaks decreasing to 1-6 per year to 1979. WJ Hadlow JAVMA 196 1676 1990.

(3) The irony of the agribusiness/deregulation diseases ushered in under Reagan-Thatcher is that today the sheep industry in the US and beef industry in the UK are hurting, the lesson being be careful what you ask for because you might get it. In the immortal words of Thatcher, 'the industry itself will out of its own self-interest take whatever steps are necessary to ensure a wholesome product, blah, blah, blah...' In fact what they do is largely determined by the ewconomic details of the government relief subsidy in place at the time.

(4) The ineffective scrapie eradication program has enabled suspicion to be shifted for incidents of US TME off cattle to the weaker sheep industry. Here's more of that "evidence" supporting the USDA view that scrapie caused the Stetsonville double outbreak [RF Marsh et al. J Gen Vir 72 589-594 1991].

"In April 1985, the owner of a mink ranch in Stetsonville, Wis., USA called the Ranch Service to report that many of his animals were behaving abnormally and some had died. Upon visiting the ranch [Marsh and Hartsough], it was apparent that aproximately 400 animals were showing various clinical states of TME." [first described in 1965 by Hartsough and Burger, JID 115 387-392 1965].

"The earliest signs were behavioural changes, in which the mink appeared to be hyperexcitable and no longer deposited faeces in a single area of the pen but distributed faecal material randomly throughout the care. Arching of the tail over the back in a 'squirrel-like' manner was observed in many animals. Mink at more advanced stages showed locomoter incoordination, as evidenced by the inability to climb into their nestboxes or to maintain their hindquarters in a straight sagittal plane when at rest. Some mink appeared completely somnolent with their noses in the corner of the cage as if in a trance. The length of clinical illness varied from 2 weeks in some mink to 6 weeks in others."

"The disease persisted on the ranch for 5 months. Of the total breeding herd of 7300 adult animals, approximately 60% [4,380] developed clinical signs and all of these died. The morbidity rate was slightly higher among females than males. The incidence of disease in the three colour phases on the farm (Violets, Pastels, and Blue Iris) appeared to be equal, as was the incidence in the first year breeders, born in May 1984, and older animals. A group of 600 Blue Iris mink received from another mink ranch on 17 July 1984 remained unaffected. Kits born to affected mothers did not develop the disease, as has been observed previously in other reports of natural TME."

"Because studies of previous occurrences of TME had indicted that some unknown contaminated feed ingredient was the source of infection, the ranch owner was carefully questioned about the mink ration formulation; he used commercial sources of fish, poultry and cereal. Most of the fresh meat portion of the ration came from fallen and sick dairy cattle whilch were picked up within a 50 mile radious of the mink ranch and returned for processing (butchering, grinding, and freezing); a few horse had been used. Sheep products were never fed to the mink and there were no feed supplements of meat and bone meal." [!!!]

This leaves us with mad cereal disease, mad fish disease, mad chicken disease, mad horse disease, or mad cow disease as the origin of this outbreak of TME. Scrapie is eliminated. Scrapie-in-cattle is also eliminated [Cutlip 1997, Robinson 1994, etc] for known strains, though it remains a valid hypothetical human health concern in its own right. TSEs have never been observed in cereals, fish, chickens, or horses: you note that some sort of mad cow disease is the most likely interpretation.

In other words, until the USDA gets a bona fide BSE monitoring program going, we have to rely on mink being the "canary in the coal mine." Mink haven't proved particularly susceptible to oral scrapie or scrapie-in-cows but mink are good "indcator species" for oral doses of other strains of TSE in the US feed supply as well as for experimental UK BSE; nothing gets the attention of a rancher faster than the loss of 4380 adult animals. With mink monitoring, it is overall effective transmissible titre that is being monitored rather than assumption- and strain-dependent histological expectations.

Some people think CWD deer and elk are also a monitoring system for TSEs in winter feeds, game farms being like mink ranches. This is less than ideal and it is completely murky what started CWD in 1967 and whether anything in the feed is keeping it going or giving rise to independent outbreaks.

The Stetsonville incident is fascinating not only in that it bears no resemblance whatsoever to scrapie or experimental scrapie-in-cattle [1997 Cutlip, 1994 Robinson, 1991-92 Marsh etc.] but also in that the downer cattle feed pool at that time apparently contained two distinct strains of TSE, hyper and drowsy in mink, that were later separated by virtue of differing incubation time and different proteolytic end points. These are both distinct from the British BSE strain [MM Robinson et al.1994]. Note too that the mink rancher was not using MBM pooled from thousands of animals from all over but individual dairy downers within a 50 mile radius. So cattle, like every other species studied, evidently have quite a few strains of BSE. Are we supposed to be surprised by this?

Stetsonville was a narrow window of time that closed 12 years ago. Evidently downer cows were separated out for mink feed as required and nothing known or investigatable supports contamination of the human food chain, much less knowingly, and no CJD cluster [which would not likely be nvCJD] has ever been associated to Stetsonville.

What are policy implications of Stetsonville: none. Those cows are water over the dam and today the US has a partial cow-to-cow feed ban in place. We do not need Stetsonville to know it is prudent to stop all rendered meat feedback loops. We already know from the Gibbs Principle to expect a background of one per million cases of bovine TSE in the US (and everywhere else) from background mutations.

The EU might restrict imports to TME-free countries but few outbreaks have occurred worldwide, none in the US since 1985 that I know of. I don't have the last year for Toronto or Blackfoot, Idaho. Not enough countries raise mink at any scale off downer cattle for it to be consistently applied.

The five US outbreaks on 11 mink ranches were in 1947 (Hayward, Wisconsin), 1961, 1963, 1963, and 1985. Three of the outbreaks occurred in large mink production facilities with on-site preparation of feed from non-ambulatory [downer] cattle [Hartsough et al, JID 115 387-392 1965].

Hayward is about 40 miles SE of Duluth, Minn whereas Stetsonville is NW of Wausau on Route 13, about 130 road miles away from Hayward. Recall scrapie was first reported in Michigan in 1947, (I believe) in the Lower Peninsula many hours and 3 states away. Rev Sci Tech 1992 Jun;11(2):491-537 ?

If you believe that 1947 Hayward or the 1961 or 1963 mink outbreaks were also bovine TSEs, then the 22 Dec 1984 Midhurst, West Sussex case loses its place in the history books even though it edges out Stetsonville by 4 months.

I wish the USDA would start to say, "there has not been a case of bovine TSE reported in the US....lately."

They bug me by constantly saying that the 'US has never had a case of BSE' as their shortened version of saying 'UK BSE has never been _reported_ in the US but we didn't look too hard and even that we mostly did in the wrong places mostly with the wrong methods plus we have reason to believe that US cattle have carried other lethal transmissible prion diseases (bovine TSEs) at various times in the past that could be much more significant quantitatively than any missed UK BSE and that these strains have different presentations from UK BSE and readily crossed the species barrier to many species including primates, with different symptoms than UK BSE and possibly nvCJD, and our current partial cow-to-cow feedback loop could lower, but not prevent, amplification of any contemporary US TSEs.'

The EU couldn't restrict imports based on this -- every country in the world is in the same boat. The US consumer evidently doesn't give a hoot about colorectal cancer, heart disease, or stroke as far as changing dietary practises go, despite a million lectures from health authorities, so what can be expected from an obscure hypothetical risk for which reductive steps have already been taken?


"In my experience, the old scrapie eradication program actually promoted the spread of scrapie. The old program was summarized by Dr. George West (Vet with the California Dept. of Food and Ag.) as: "kill all the sheep, burn down the buildings and roll up the wire." This program was VERY effective in reducing the REPORTED incidence of scrapie.

What happened over and over again in purebred Suffolk flocks is that at the first hint of a scrapie problem, the owner would have a flock dispersal sale rather than endure the Scrapie Eradication Program, and scrapie sheep would be introduced into previously clean flocks. This happened to several clients of mine, who thought they were geting good deals on genetics which had previously been out of reach.

It is important to remember that scrapie in the U.S. is almost entirely a disease of blackface (Suffolk and Hampshire) sheep.

It is quite a leap from experimental brain innoculation transmission to the assumption that natural transmission occurs from small ruminants to cattle. Scrapie is neither common nor widespread in the U.S. The U.S. sheep industry is tiny in comparison with the cattle industry. (yearly per capita consumption of lamb meat in the U.S. is in the range of 2kg or so).

I see, on average, one case of scrapie every 3-4 years, and I practice in the county with the largest sheep population in California. In fact, sheep carcasses *are* wasted. When BSE first became known, rendering plants stopped accepting dead sheep and all of the offal from the slaughter plant in Dixon, California was trucked to a hazardous waste dump (Kettelman City, Calif.), increasing the cost of processing lambs and further depressing a moribund U.S. sheep industry. Most dead sheep around here are rendered by Mr.Turkey Vulture.

I think the mink story is more plausible evidence for cattle S.E.s in the U.S."

Paul Michelsen,M.S., D.V.M.
Potter Valley, CA 95469


After harvesting the pelt, is the carcass fed back to mink? This could result in amplification of any TE existing in the mink. Also, there could be significant cannibalism at high stocking levels. . Littermates also bite each other.


There is nothing in the full text of the original interview with the farmer that supports this scenario, which in any case addresses possible amplification, not the origin of the TME. There are too few mink for the 'one in a million' event. Experimentally, both strains passaged quite easily to cows, with difficulty to sheep and to closely related ferret. One strain, drowsy, was a minor component and difficult to passage in mink themselves.

Marsh grew up on a mink farm near McMinville, Oregon plus worked for the Wisconsin Ranch Service, so was thoroughly familiar with mink behavior and mink ranch practices. Early papers discuss cite kuru, the celebrated instance of transmission by cannabalism. Marsh published 29 papers containing 'mink' in the title, 16 of these were prior to Stetsonville including his earliest papers from 1969. TME was first descriped 4 years earlier in J Infect Dis. 1965 Oct; 115(4): 387-392 and 393-399 by Hartsoughg GR and Burger D; the earliest known outbreak was 1947 in Hayward, Michigan. Veteran pathologist WJ Hadlow described the Ontario Canada outbreak in Can Vet J. 1968 Aug; 9(8): 193-196.

I don't believe they do feedback on large US mink farms because of risk of spreading other diseases and concentrating reproductive toxins such as fish PCBs and the utterly insignificant amount of meat per year and its abrupt seasonality. Feeding carcasses back to the mink may still be a common practice in some remote farms, but not as a rule. Many mink are now fed very special diets.

There was a very brief window of infectivity and no subsequent outbreaks on this farm. 600 animals of a susceptible breed purchased from a second ranch shortly thereafter and raised on the same subsequent food did not acquire TME. Transmission to kits was not seen.


Pigs were not mentioned as a possible feed source to mink -- was this likely?


Doug Anderson Darlington International Long-term Wisconsin resident and friend of Richard Marsh
Pigs were very rarely ever used as the cattle were easier to remove the meat from. Usually only cattle meat and some organs (liver, kidney, heart) as the ranchers wanted the mink well fed. Mink are tremendous cannibals and will eat their kits if not removed from them shortly after weaning. Sometimes even that is too late.


Would be a concern over Aleutian disease so that rendered mink would be avoided?


This was a question in 1985 that I never got a good answer for. In 1965 it could have easily been the case. Since their was no subsequent re-infection in 1985, the prospect of another source needs to be hypothesized. One of course is the cannibalism, one is a concentrated dose of an agent causing rapid infection, whether the agent was a tse that replicated, or an external source causing the infection may never be known. Isn't it strange that the time frame is the same as the UK BSE outbreak? Also I have never received a good explanation discounting the organo-phosphates as a chemical source of mutation


Is the mink farm still going, was 1985 the end of it?


I do not know if Stetsonville is still a mink farm today, but have friends that could confirm it. 1985 was the end as there have been no cases since. Mink are still fed cattle meat today in many locations, and are fed some exotic blends in others. I believe most all contain animal proteins as they have through the years.

A Sorry Sight: Does the way we manage cull cows give the industry a black eye?

October 1995 by Nita Effertz   Beef Today -  Farm Journal 
"Hey, bid alright, sir . . . step right up we're gonna sell this fine cow. I've got a 5 dollar bid on a cow, a good cow, who'll give me ten . . . Walking on three, milkin' on two . . . You ain't got ten, I ain't through. Cause I'll take eight, give me eight . . . This cow's great . . . One big foot and one bad ear What do you care if she can't hear! Nothing wrong that you can't fix . . . You won't give eight, I'll take six! Six big bills, c'mon try . . . She don't need but one good eye. What do you mean she ain't alive! See her breathin' . . . I'll take five. C'mon boys, you make me sore CALL THE VET . . . I'll take four! Four ain't much, she's just a pup . . . C'MON PREWITT, GIT 'ER UP! C'mon boys, nothin's free . . . GIT THE TRACTOR . . . I'll take three! Three is all I'm askin' now . . . Surely someone needs this cow! You may think that I'm all through . . . There's still a chance . . . I'll take two! PREWITT, GIT 'ER PROPPED UP STRAIGHT . . . LEAN 'ER UP AGAINST THE GATE! Fine replacement, bled and pregged . . . Pay no mind to that bad leg. She's a dandy, not too old . . . Tits'll grow back so I'm told . . . Rigor mortis? . . . No, just tense . . . Someone give me 50 cents! Anybody give a dime? Hurry up! There ain't much time! C'mon boys . . . use your head . . . DAMMIT, PREWITT, NOW SHE'S DEAD!" --Baxter Black, "Sellin' Prewitt's Cow" Reprinted with permission from "Coyote Cowboy Poetry"
It's to beef producers' credit that most don't wait quite as long as Prewitt did to market their cull cows. But late or untimely marketing still costs cattlemen millions annually. What's worse, delaying marketing until culls are too thin, too weak or too diseased is setting this industry up for an even costlier calamity with consumers.

Consider "cancer eye"--bovine ocular neoplasia. Marketing cows with advanced stages of it costs this industry $14.5 million a year in condemnations. "But a bigger problem is that this is a public perception issue ready to explode," says Chris Kukay. Kukay was a member of a team of Colorado State University researchers that last year conducted interviews and on-site audits at 21 packing plants across the country to document the cull animal marketing problem.

The resulting nonfed beef audit found that quality defects cost $69.90 for every cow and bull marketed. Much of that was chalked up to producers' passing their problems down the line by marketing cull cattle in poor condition. One major packer representative interviewed by the audit team deplored the lack of accountability: "Nonfed cattle go through too many hands--nobody cares, nobody's responsible, nobody communicates backward or forward--with little chance of traceback of problems."

"Whereas all segments of the industry are responsible for the high incidence of bruising [more than 30% of cow carcasses have major bruises], the producer is wholly responsible for preventing advanced cases of [cancer eye], emaciated cows and those with infected prolapses," notes Colorado State livestock handling expert Temple Grandin. "Marketing animals when they are debilitated or physically unfit costs the beef industry almost $12 a head for every cow and bull marketed. Yet prompt marketing is all it takes to keep mildly disabled cows from becoming 'downers.'"

Data gathered in nonfed packer holding pens found a "downer cow" incidence of almost 1%--twice Grandin's earlier estimate. The audit found severe cancer eye in 2% and extreme cancer eye in 1.6% of all beef cattle--more than 108,000 head a year. That too is twice previous estimates.

"These are cattle that should never arrive at a packing plant in this condition," says Grandin. It's likely only 10% of the producers cause 90% of the problem, she believes, but the majority needs to start policing the minority.

Producers are now being asked to euthanize severely disabled cattle and those with advanced cases of cancer eye at the ranch. "The good auctions kick them out," notes Grandin, "but there's always some 'Joe's half-dead truck' that will take them around to the few plants that still accept them."

"If you've waited that long to market, there's very little and often no value left in the animal," says Kukay, "and it could actually cost you $30." Indeed, many major auctions are now euthanizing disabled cattle on delivery--at the producer's expense.

Almost all the problems the audit found in salvage cows and bulls could be corrected or minimized by more timely marketing, according to CSU's Gary Smith, who headed the nonfed audit project. "When a cow's productivity goes downhill, get her to market. When you know her teeth are gone, when she's a little lame or her eye isn't responding to treatment, get her to market."

Timing could also reduce bruising. With bruising evident on almost 80% of all cow carcasses, it's a problem that costs the industry over $30 million a year. Cattle that aren't marketed until they are very lame become weak and are more susceptible to bruising during handling and transport. The audit found nearly 3% of beef cows and more than 7% of beef bulls were severely lame when marketed. And a Canadian study showed most lame or downer cattle are in very bad condition before leaving the farm or ranch.
Regardless of when you sell, refocus efforts on more careful handling and loading. "Nonfed cattle sometimes are handled far too roughly . . . far too many are bruised, have dark cutting beef or suffer bone breakage because they are not carefully loaded, driven or unloaded as they move from farm or ranch to market," one major packer told the nonfed audit team.

According to Grandin, there's an optimum density for a load of cattle. "Don't overload. One or two extra cattle is all it takes to double bruising," she says.
The nonfed audit team also developed a strategy for reducing cancer eyes. "We found 95% of all cancer eye cases were in Hereford-marked cattle," says Kukay, "with Simmental-crosses noticeable in the remaining 5%." Five pieces of cancer-eye advice: * Breed stock with dark eye pigment. * Have suspect cancer-eye lesions treated by a veterinarian, and schedule a re-exam for two to six months later. * Cull animals not responding to treatment. * Cull offspring of animals that have been treated for cancer eye. * To avoid negative public perception, don't try to salvage cattle with advanced lesions. Euthanize them at the farm or ranch. .

Economist: Don't Blame Oprah

The Associated Press By MARK BABINECK 20 Feb 98 AMARILLO, Texas (AP) - An economic expert testified today that factors such as drought, high corn prices and weak exports had far more impact on a cattle market slump than anything said on Oprah Winfrey's talk show.

``This (declining market) was already happening in response to a drop in consumption in Southeast Asia ... not regarding anything to do with what happened on this show,'' said Marvin Hayenga, an Iowa State University agricultural economics professor.

A group of Texas cattlemen claim that a market plunge following Ms. Winfrey's April 1996 talk show on ``dangerous foods'' cost them $12 million. They're suing her, her production company and vegetarian activist guest Howard Lyman.

Part of the show centered on mad-cow disease, which has stricken British herds since the 1980s. A related strain of a similar human ailment is suspected of killing 23 people there.

No cases of mad-cow disease have been reported in the United States. [Really? See the papers below from Prof. Marsh. --webmaster]

In his second day on the stand, Hayenga, a defense witness, said cattle prices were dropping before the show even aired. Hayenga also targeted cattleman Paul Engler's assertion he lost more than $4 million by selling cattle on the futures market because he was spooked by the episode. Hayenga testified Engler waited too long after the show - two weeks or more - to ``hedge'' by selling futures.

``If the show is cause for this particular action in the futures market, in my view it needs to be much more immediate,'' Hayenga said.

Bovine spongiform encephalopathy in the United States.

J Am Vet Med Assoc 1990 May 15;196(10):1677
Marsh RF
Department of Veterinary 
Science, School of Veterinary Medicine, University of Wisconsin 

Bovine spongiform encephalopathy: a new disease of cattle?

Arch Virol Suppl 1993;7:255-259
Marsh RF
Bovine spongiform encephalopathy (BSE) was first recognized in Great Britain in 1985. Most believe that the disease is of recent origin initiated by feeding rendered animal protein from scrapie-infected sheep to cattle, then perpetuated by feeding rendered infected cattle to other cattle. This paper explores an alternative hypothesis that BSE existed in cattle populations in an unrecognized form for a much longer time until amplified by changes in the rendering process that allowed cattle to cattle transmission to occur.

This viewpoint is supported by observations that transmissible mink encephalopathy, a disease that first occurred 45 years ago [so in 1948], is likely caused by feeding downer cows to mink, and that the sporadic form of Creutzfeldt-Jakob disease occurs spontaneously with no evidence of natural transmission. This epidemiologic scenario on the origin of BSE has important implications for prevention of the disease in BSE-free countries. Mainly, emphasis needs to put on practices of feeding animal protein to cattle rather than in reducing the prevalence of sheep scrapie. If BSE is already present in the cattle population, the major threat becomes feeding cows to cows.

Combating mad cow disease in the United States.

Public Health Rep. 1997 Sep; 112(5): 357-358.  
Henderson DA.      

Scientists offer cattle methane solution

Wednesday, February 18, 1998  ENS
For more  information, contact Dr. Graeme McCrabb, CSIRO, 07 4923 8193
Researchers have found that the amount of methane produced by a cow varies dramatically depending on the quality of its diet.

Putting cattle on a high-quality grain-based diet results in more meat and milk production as well as a reduction in greenhouse gas emissions, according to a team of Australian and Japanese scientists. Cattle generate around 15 to 20 percent of all the methane produced as a result of human activity -- up to 100 million tons a year. Methane is 25 times more potent than CO2 in causing global warming.

Research by a joint team led by Dr. Graeme McCrabb of Australia's federal science agency, CSIRO Tropical Agriculture, and Dr. Mitsunori Kurihara of Japan's National Institute of Animal Industry, has identified a way both to cut gas emissions and to lift production of meat and milk -- especially in the tropics, where at least half the world's cattle herd resides.

The methane is generated by bacteria in the cow's stomach breaking down the fodder which the animal has consumed. On average, 6 to 7 percent of the animal's total food intake is turned into gas and each beast puts out between 60 and 113 kilos of methane a year. The researchers have observed that the amount of methane produced by the cow varies dramatically according to the quality of the diet it is fed on -- animals on poor quality feed, which is common in warm climates, generate a lot more gas and produce less meat or milk. They also found that better quality diets led to improved production from the animals -- faster growth rates and a greater overall yield of milk and meat.

"It's perfectly logical -- the energy that is being wasted as gas emissions from animals on a poor diet is instead converted to production in a balanced, high quality diet," McCrabb says. "We found cattle on a forage diet produced four and a half times as much methane for every kilo gain in liveweight as cattle on a high-quality grain-based diet."
The research offers the prospect of substantial gains in efficiency for the Australian northern beef cattle herd -- while at the same time lowering the national level of greenhouse emissions in a meaningful way, he says.
"This research indicates it is possible not only to reduce methane emissions from ruminant animals such as cattle and goats in the tropics, but at the same time to increase total food protein output, and so improve the diets of millions of people."
The world currently has 1.33 billion cattle and 1.1 billion sheep and goats, predominantly in the tropical and subtropical regions, and subsisting on poor diets. India has the largest cattle herd, followed by Brazil and China.

Europe could face 'devastating' outbreaks of animal diseases

February 18, 1998 By MICHAEL SMITH, The Financial Times
BRUSSELS -- Europe faces "devastating" animal disease epidemics in the future and should alter its strategy for containing them, the United Nations Food and Agriculture Organization warned Tuesday.

The agency called for a cut in herd concentrations, an increase in border controls and the development of animal identification systems.It also suggested the private sector be obliged to take on some of the costs of containing diseases and warned governments that the privatization and decentralization of national veterinary services could reduce their effectiveness.

The agency's recommendations are aimed at containing fast spreading diseases such as swine fever and foot and mouth disease, rather than the BSE "mad cow" disease, which develops more slowly.Europe has suffered more epidemics than any other region.

Nine of the 15 major epidemic livestock diseases recorded internationally have occurred in Europe. The FAO blames dense populations of livestock and an increase in long-distance animal transportation as trade increases. Both trends stimulate the rapid spread of disease.Farms in Belgium, the Netherlands and Germany concentrate up to 3,600 pigs per square mile of land.

"This causes increasing pollution and should not be tolerated any more," said Yves Leforban, FAO health officer.The Netherlands, affected last year by a costly outbreak of swine fever, and Denmark are among countries already taking steps to cut animal densities. Eastern European countries are less of a problem because farming is less intensive there.

In a report Tuesday the FAO challenged the practice by which the public sector in Europe bears the cost of epidemics and compensates the private sector for losses incurred.It argued this did little to encourage sanitary methods.

"Industry does not appear to be able to discipline itself and it may be that government compensation instills false security."The FAO suggests a compulsory insurance program for livestock owners to protect against the costs of disease. It said certification and identification of animals were essential for their safe movement.

Two held in New York subway anthrax scare

[This story turned out to be essentially fraudulent, as did an even more inflammatory later NY Times story. It apparently had to do with stirring up public fears of terrorism at a time that support was sought for the bombing of Iraq. The FBI informant in Las Vegas turned out to be a convicted extortionist seeking to swindle two befuddled paramilitary blow-hards, one of whom had legal anthrax vaccine. The NY Times apparently fabricated entire sections concerning NY subways , SwAT teams in black, and aerial surveillance of Las Vegas. However, such an anthrax scheme could be carried out and spores in the ground are still a risk for cattle in UK.]

TWO white supremacists were arrested in Las Vegas yesterday, accused of a plot to release anthrax spores into a public place, possibly a subway system. Aurelio Flores, of the FBI, said that the men belonged to the Aryan Nations organisation, a racist group based in Idaho which aims to "preserve and protect the white race".

Mr Flores described the matter as serious: "These individuals were involved in the construction of a weapon. We have no idea where they were going to use it." FBI sources in New York, however, suggested that their city was the likely target and that the men intended to attack the subway, copying the Japanese doomsday cult that killed 12 people in Tokyo in 1995.

The arrests came as the American security agencies are particularly alert to the threat of biological attack, and specialists from the Pentagon and the FBI were sent to examine the substance believed to be anthrax yesterday.

The men - Larry Wayne Harris, who was put on probation last year after obtaining bubonic plague bacteria through the post, and Billy Levitt - were kept in isolation cells and examined by doctors before appearing in court.

Aryan Nations, which is based in Hayden Lake, Idaho, has been linked to bombings, murders and bank robberies. Founded in the mid-1970s, its compound is home to the Church of Jesus Christ Christian and its political organisation.

The church believes that America's white Christians are the people referred to as Jews in the Bible; that Jews themselves are the children of Satan and that black people are dehumanised as "mud people". The political arm holds that America is the true Israel and the country is being denied its destiny by ZOG, the Zionist Occupied Government in Washington.

Landlord faces jail for selling T-bone steaks

February 20 1998 Times BY MICHAEL HORNSBY  
A PUBLICAN has become the first person in England to face prosecution for breaching the beef-on-the-bone ban. Alan Coomber, landlord of the 12th-century Bell Inn at Iden, East Sussex, has been serving his customers 16oz and 28oz T-bone steaks, at #12 and #17 each, since the ban was imposed on December 16.

A blackboard outside the inn invites passers-by to come in and try "The Big One". After a visit by health inspectors posing as customers, he has now been told that he can expect to be summoned before a magistrates' court where, if convicted, he would face a maximum punishment of a #5,000 fine or six months in prison or both. A hotelier in Scotland is to appear in Selkirk Sheriff Court on March 10 charged with the same offence.

Despite the threatened prosecution, Mr Coomber was yesterday still serving the banned fare.

"T-bone steaks are our speciality," he said. "We get tourists from Holland, Belgium and Germany coming here to buy them. It is a big part of our business. We sold two T-bones today and will probably sell about 15 at the weekend. If I thought hundreds of people were going to be dying, obviously I would not be doing this. But everyone knows the risk is as good as non-existent. All I and my customers are asking for is the right to choose."
The Beef Bones Regulations were introduced by Jack Cunningham, the Agriculture Minister, after he was warned by scientists of a remote risk that nervous tissue attached to cattle bones might be infected with "mad cow" disease. A statement issued yesterday by David Powell, chief executive of Rother District Council, said the council would have been "guilty of maladministration if it did not investigate and take appropriate action".

Mr Coomber said:

"I shall stand there and take my punishment. I would not want to go to prison, but we would not want to stop selling T-bones. I do not think they would send me to jail. We sell only the finest British beef. I have it delivered from a regular supplier in Wiltshire."
Another prominent beef-on-the-bone rebel, Paul Robinson, who runs a family butcher's shop in Stockbridge, Hampshire, yesterday abandoned his campaign of defiance after being warned that he would be prosecuted if he did not.
"I sat down with my brothers and we decided that we could not put the business and the livelihoods of the 14 people we employ at risk," Mr Robinson said. "So I now have to have a notice in the shop saying 'all beef displayed on the bone has to be boned before purchase'."
In the Commons, Jeff Rooker, the Food Safety Minister, brushed aside calls for the beef-on-the-bone ban to be lifted, braving ironic cheers and laughter from Opposition benches.
"We are being asked by the Opposition to knowingly allow for the first time BSE infectivity into the food chain", he said. "We are not going to do it now and we are not going to do it in the future."

Mad Cow Home ... Best Links ... Search this site