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Pattison: epidemic worries are over
Pattison claim doubted
Scrapie and BSE epidemic in Norway
Sheep-dip ailment acknowledged
Agribusiness seeks to weaken organic food laws
New cow case in France

Pattison: epidemics are almost over

Daily Telegraph of 4 February 1998
speech by Sir John Pattison to the annual meeting of the National Farmers' Union.
FEARS of an epidemic of human brain illness arising from mad cow disease were dismissed yesterday by the Government's scientific adviser.

Prof Sir John Pattison, chairman of the Government's independent Spongiform Encephalopathies Advisory Committee said new cases of BSE in cattle were plummeting and cases of a related fatal brain illness in young people were occurring only in low numbers.

He told the annual meeting of the National Farmers' Union of England and Wales in London that 1998 would be a "turnaround year" for mad cow disease.

Only 23 cases of new variant Creutzfeldt Jakob disease had so far been reported. Of these, three were recorded in 1995, 10 in 1996 and 10 in 1997. It was this new variant of CJD which provoked the Government's warning statement in March 1996 that sparked the beef crisis and the European Union ban on exports of beef.

Sir John estimated that the number of deaths expected from the new variety of CJD, which has been linked to the cattle illness, would be far fewer than feared.

Given an estimated incubation period of between 10 and 15 years for this human brain disease, he expected casualties to be somewhere between 100 and 1,500 - compared with up to 500,000 which some experts feared two years ago. He took the view that the final total would be at the lowest end of that scale.

New cases of BSE in cattle were expected to fall from 4,197 last year to 1,741 this year, he said. These would fall to about 89 by 2000.

"I think the end of 1997 marked the bottom of the problem and we can only go up from now," Sir John said. "I have no doubt that the BSE epidemic is fast disappearing and that the number of new variant CJD victims is not rising rapidly.

"As cases of new variant CJD remain low, this will eventually mean that the whole problem of the regulations we have in place will disappear altogether. I believe we will be saying over and over in 1998 that there is no threat from beef or beef products reared in the United Kingdom." Sir John said.

Consumers, he said, had changed their views on beef over the past 12 months and this was indicated by the critical reaction to the Government's controversial decision to ban the sale of beef on the bone to protect consumers from the slight risk of contracting CJD. But he defended Jack Cunningham, the Minister of Agriculture, for deciding to ban beef on the bone.

Farmers and consumers had to understand that the Government's main aim was to re-establish exports of beef which were so vital to British farmers.

Anyone in Mr Cunningham's position would have found it difficult not to take action to show Europe that everything possible was being done to make sure that Britain's health and hygiene controls on meat were the tightest in the world.

Sir John admitted after the meeting that some members of his committee were more cautious than himself.

"There is always a chance that the estimates I have given are wrong. Some members are more cautious than I am."

Pattison claim doubted

5 Feb 98 webmaster opinion
No question that clinical BSE cases are dropping with the incineration programs in plac for high risk cows. We do not yet have information about infectious titre levels in the overall herd. Remember, the clinical state of the cow comes very late in the process. This was the basis for the recent ban on all cuts of meat containing bone.

The other issue has always been, are we going to get another scrapie or chronic wasting disease situation, where the disease lingers on ineradicably for decades in elk and sheep or centuries in sheep. If not, why not?

No one can have the slightest idea of the scope of the nvCJD epidemic based on information released so far. There is no understanding whatsoever about what is so special about the current victim set within the met/met at codon 129, and so no understanding whatsoever about what they imply. I see no support at all for the victim group having had exceptional exposure levels within their age/genetic cohorts, quite the contrary. So why them?

It is only when additional speculations are made about the representativeness of this group that guestimates can be made about the scope of the epidemic. For example, they could reflect the entire UK population of some rare dramatic overproducer allele that is preferentially expressed in somewhat younger people. The main epidemic could be 5-10-15 years off and we haven't even seen the leading edge of it yet.

Until Pattison comes up with a scientfic rational for the current set of victims -- and I don't hear even a hint of this -- I have to put his remarks down to reassurance and market concerns. The timing suggests that it is negotiating fodder for the upcoming WHO meeting this month in Geneva.

Finally, there is the matter of resolving L108F and T189V. These always come together as a packet here; it is completely unknown, say, whether they work in synergy, in opposition, or in neutrality. For all we know, 189V is completely resistant and 108F has a ten day incubation period. The mouse genetics paper in the February 1998 issue of Nature Genetics shows precisely the fatal fallacy in what Pattison is trying to do in predicting the nvCJD epidemic. Think of the data in mice terms:

Let us say we have lost 23 mice of genotype 129/Ola gtB/gtB with incubation period 133 days.

Please tell us what the incubation period will be in 129/Ola L108 189V/L108 189V mice.

Hard to bootstrap off that 133 days incubation period, isn't it?

If you can't do it in co-isogenic mice with simultaneous equivalent inocula, how can you do it in a highly heterogeneous human population with unknown inocula?

The danger of Pattison's perspective is induced complacency. I think we will know a whole lot more about how the infection is progressing in the general population by the end of the year using 15B3 antibody to rogue prion with random accident victims and dementia cases.

The default assumption is that essentially all 60 million people in the UK are infected. The issue is mainly how fast the disease is progressing relative to normal lifespan and other sources of morbidity.

Further Reaction and Opinion:

J Ralph Blanchfield UK  4 Feb 1998
I share Sir John's assessment of the BSE situation.

The figures quoted in the report for nvCJD -- "three were recorded in 1995, 10 in 1996 and 10 in 1997" are of course taken from the 2 February Department of Health statistical table. They may be a suitable basis for annual statistical reports, but are a very misleading basis for considering the trend of incidence. The calendar year of death is a very crude timescale. On a shorter timescale one might note that there have been no new cases in the past two months, and only two over the past six months.

However, as pointed out in the current IFST Position Statement on BSE, the pattern so far assignable to the definite and probable cases over the period 1994 to date varies greatly according to whether one works on the basis of date of appearance of clinical signs (in cases subsequently confirmed) or (as in the statistical table) on date of neuropathological confirmation . Either way is a reasonable way of expressing the statistics over this period, provided that the basis is clearly declared.

But the latter is not meaningful for assessing trends. LaBudde (1997) has analysed statistically the dates (as best could be estimated) of onset of symptoms in the nvCJD confirmed cases up to August 1997 and found that the mean-time-between-cases appears constant at 7 cases/year up to that point, with no evidence that the rate was increasing. However, neither way of expressing the statistics provides a means for long term forecasting of likely future incidence. This is because of the small number, unknown variations in incubation time, the absence until now of a means of early diagnosis, and variations in the duration from clinically-observed onset to death/confirmation.

The incubation time is not only unknown, but, assuming the likelihood of a causal connection, is likely greatly to vary inversely to the ingested dose of BSE infectivity and the susceptibility of the individual.

I hope that Sir John is correct in his long-term nvCJD forecast. I would be inclined to share it if the pattern of the past six months continues for the rest of 1998 and into 1999. But for the present I think it is too soon to forecast, and I share the caution of "some members of his committee".

Roland Heynkes, Germany Thu, 5 Feb 1998 
The Pattison statement is typical for him. Not the governmental statement, but BSE and its transmissibility to man is the reason for the beef crisis.

There is no scientific basis for this estimation of expected deaths from nvCJD, which is nothing else then a lobby action. There is no scientific reason to estimate an incubation period of between 10 and 15 years for CJD or even vCJD. Observations from iatrogen cases and simple mathematical calculations show that it can be much longer.

New cases of BSE in cattle are down as a result of the partial ban of meat bone meal, but also of the culling program. If the older cattle are killed, they can not become ill from their BSE infections.

The significant decrease of BSE cases does not mean that BSE will disapear as soon and rapidly as Pattison estimates. The culling program manipulated the numbers and a decrease of numbers of BSE cases does not mean, that the number of infected cattle decreases similarily. Increasing incubation periods have the same effect. Furthermore the stop of canibalism did reduce the number of kuru cases, but of course only to the normal level, not to sero. The elimination of meat bone meal as source of infection will allow to see the level of other ways of transmission.

Sheep-dip settlement

February 4 1998 Times Michael Hornsby 
At one time, organophosphates were considered as a possible cause of BSE . The detailed symptoms of the farm manager would be of some interest. -- webmaster

A SHEPHERD has received 80,000 compensation for damage to his health allegedly caused by sheep dip .

Lancashire County Council has agreed to pay the sum to Robert Shepherd, 62, from Crook, Co Durham, in an out-of-court settlement of a case brought on his behalf by Unison, the public service union. Mr Shepherd was employed by the council as a farm manager at the Lancashire College of Agriculture, where he was responsible for dipping the sheep on the college's working farm twice a year. He became aware of ill-health in 1979 and his condition worsened over the next ten years until he was forced to retire in 1991.

As protests mount, Glickman postpones action on organics rules

February 7, 1998   The Associated Press By CURT ANDERSON 
WASHINGTON -- Action on new national labeling rules for organic foods will be delayed 45 days for more public comment, Agriculture Secretary Dan Glickman decided amid heavy criticism from pro-organic groups. The Agriculture Department has already received more than 4,000 comments on the rules, hundreds of them objecting to the possibility that irradiation, genetic engineering and sewage sludge fertilizer could be involved in organics. Glickman, however, noted that the Agriculture Department had taken no stand on those issues and wanted to hear from the public about them. The new deadline for comment is April 30.
"This is not a final rule and should not be read to reflect how USDA will finally resolve the many difficult issues involved," Glickman said Friday. "Our goal is to develop a final rule that the organic community and all the public can embrace."
But the mere possibility that organics rules could include a high-tech process such as irradiation to kill bacteria is anathema to most organic farmers, who say big agribusinesses seeking a share of the market are trying to move the definition away from its all-natural tradition.
"We as organic farmers and our customers will not sit idly back and have ... (the rules) force-fed to us by corporate agribusiness lobbyists and bureaucrats in Washington," said George Siemon, chief executive of an organic co-op in LaFarge, Wis. "The farmers of our co-op will not lower our standards."
Several big corporations have launched organic product lines in recent years as consumers -- increasingly concerned about pesticides and other chemicals in food -- are now buying organic food to the tune of $3.5 billion a year and growing.

The rules stemmed from a 1990 law intended to provide a national definition and label requirements for organics now governed only by a patchwork of state and private certification programs. But many organic producers say the national rules will be weaker.

"We strongly believe that the proposed rule is not compatible or consistent with current organic practices," said Kathleen DiMatteo, executive director of the Organic Trade Association based in Greenfield, Mass. "As we see it, USDA's proposed rule blurs the lines between conventional and organic agriculture."
Some other objections raised by organic farmers:

Livestock could be fed up to 20 percent non-organic feed and could be treated with antibiotics under certain circumstances. The rule does not mandate that animals get access to the outdoors.

Numerous recommendations of the 14-member National Organic Standards Board were ignored and more stringent local organics guidelines would not be allowed. Loopholes could permit use of synthetic pesticides and other materials in organic farming that have never been allowed before. Previous uses of land would not be adequately taken into account when it is certified for organic production, even if it once was heavily contaminated.

Glickman has scheduled public hearings in Texas, Iowa, Washington state and New Jersey on the organics rules and is encouraging people to forward comments via the Internet. "We want everyone to participate fully in this process," he said. The hearings are: Feb. 12, Austin, Texas; Feb. 18, Ames, Iowa; Feb. 26, Seattle; March 5, New Brunswick, N.J.

New case of 'Mad cow' disease detected in France

February 8, 1998   Agence France-Presse
PARIS - French authorities Sunday announced a new case of "mad cow" disease, the first ever in the Haute Savoie region of southeastern France. This latest case is the second reported this year in France and brings to 33 the number of cases of bovine spongiform encephalopathy (BSE) recorded in the country since 1990, the agriculture ministry said. A spokesman said the entire herd from which the infected cow came would be destroyed, adding that additional information would be provided on Monday. The last case was reported last month in the northern Manche region.

According to a European Commission report delivered to the European parliament at the beginning of the month, 13 of the 15 European Union members countries have yet to implement EU regulations on heat treatment for bone meal, suspected of spreading the disease. Paris has stated its intention to implement the EU directive, but EU sources said it has yet to do so.

According to the Commission report, only Finland and, to a lesser extent, Germany have applied the rules set in July 1996. BSE has been inconclusively linked to a fatal new strain of a degenerative human brain condition known as Creutzfeldt-Jakob disease.

Scrapie and BSE in Norway

19.1.98  Reprinted correspondence from S. Dealler site
The unidentified correspondent appears very well-informed. and honest. Only an explcit discussion of the scrapie-to-reindeer issue is lacking, presumably because this raises sensitive racial issues. --webmaster
Dear Steve,

It is true that there has been a marked increase in reported cases of scrapie in Norway in 1996. However, we have no reason to believe that these cases could be BSE-related. (We have not yet received any results from Collinge in the UK where samples have been sent, we expect results indicative of classical scrapie). Here are some facts about the TSE-situation in Norway:

DOGS AND CATS:

One case of spongiform encephalopathy was reported in a Norwegian cat (Vet Rec 29 April 1995, Ueland and Wells). The case was confirmed as BSE in a UK laboratory. The only feed import from the UK to Norway has been petfood, and the most likely explanation is that the cat may have been fed British petfood.

Last year, there was a suspicion of BSE in a dog. However, this suspicion was not confirmed when samples were sent to the UK. I do not know what kind of tests were done in the UK.

SCRAPIE:

Total ovine population: 2.500.000 of which 1.000.000 winterfed sheep in 24.000 flocks (approximate figures). There have been a total of 52 cases of scrapie in Norway since the first case was diagnosed in 1981 (approx. 0,2% of 24.000 flocks). Over half of these cases were reported in 1996 (31 cases). In 1995 we had 8 cases, and 5 cases were reported in 1997. In all other years since 1981, there were at most 1 or 2 reports per year.

The disease has been reported in four of the 19 Norwegian counties. The majority of cases are concentrated in two adjacent counties, Rogaland (61 %) and Hordaland (31%), in the south-western part of the country. The county of Sogn og Fjordane had 2 cases (last in 1985) and the county of Nordland 2 cases (one in 1996 and one in 1997).

Probably one reason for increased reporting is increased knowledge and awareness about symptoms of scrapie among veterinarians and sheep-owners. I believe one case was even discovered by a tourist who had rented a mountain cabin and observed strange behaviour in a sheep. Most cases are from the same 2 regions and are probably a result of trade or other contact between flocks in these areas. There has for many years been a ban on movements of sheep from one county to another.

A national test program has started. Many brains (3000 ?) from sheep over 3 years old from all counties in Norway will be examined yearly. In addition, all sheep and goat flocks will be visited once yearly forclinical examination. Sheep-owners will receive information on scrapie and will be shown a video on symptoms. I do not think this is done in any other european country, with the exception of Iceland. (I would like to ask you about what kind of screening is done in the UK, do they know the UK-incidence of scrapie and has MAFF started to sample scrapie-brains from flocks where there is a past history of feeding with ruminant proteins ? I believe there must also be quite a lot of scrapie, and possibly BSE-variant-scrapie, in France. I worked as a vet pathologist in France from 1979 to 1987. France has imported great quantities of MBM from the UK, scrapie became notifiable in France only in 1996 and french sheep may have received ruminant protein feeds until 1994.)

TME

N.B. About 50 % of Norwegian mink farms are situated in the county of Rogaland and fur animals have been fed raw waste (including heads/brains) from cattle and sheep for many years. No case of TME has ever been reported in Norway.

CWD

No case of CWD has been seen in Norway.

BSE

No case of BSE has ever been reported in Norway. Feeding of ruminants with ruminant protein (except milk proteins) has been forbidden since 1990. Rendering procedures for animal waste require since july 1994 a minimum heat treatment of 133 degrees C under pressure 3 bar for at least 20 minutes. Earlier regulations ensured a minimum treatment of 120 degrees for at least 20 minutes.

Production and use of meat and bone meal:

In 1990, Norway produced approx 30.000 tonns of MBM, enough to cover national needs. MBM was traditionally used as an additive in feeds for poultry and pigs. It was unusual to add MBM to cattle feed. During 1989, production started to exceed national needs and interest for the use of MBM for ruminants thus increased only about one year before the ruminant-protein ban.

Imports

Norway has until 1994-1995 had a very restrictive import policy for live animals and animal products. Very few import permits have been granted for live sheep and goats, and only for animals from New Zealand. Before 1991, there were very few imports of live cattle. Cattle from the UK have been imported only between 1982 and 1986. During this period, a total of 10 UK-cattle were imported. All these animals were slaughtered long before 1996. The 3 importers have been traced and the progeny og these animals will remain under surveillance. From other countries known to be BSE-infected, there has been only one import of cattle. This import was from France, in 1997. Approx 1200 cattle for breeding were imported during the years 1991-1996. Most of these animals were from Denmark and Sweden, some were from Finland and Austria. There have been no imports of cattle or sheep for slaughter from any country. There were no imports of beef from the UK before the 1996 ban.

Norwegian import statistics indicate no imports of meat and bone meal (MBM) as animal feedstuff. Before July 1994 (EEA-agreement with the EU) there was a general ban on imports of animal products and products such as MBM could only be imported if exemptions were granted by the vet authorities. Until 1.1.95 (WTO-agreement) Norway also had a monopoly situation with only one importer (Statkorn) for grains and feeds for farm animals. After 1.1.95, imports of feeds still remain easily surveyable, since there are at present only 4 importers of feeds for ruminants, swine and poultry. None of these 4 importers have had any import of MBM from the UK or from any other country. Also, the customs fee for imports of MBM after the WTO-agreement would be very high, discouraging such imports even at low purchase prices. I have talked on the phone with each of these 4 importers and they only import vegetable proteins for animal feed. They say it would be unthinkable for them to import MBM from the EU, even though this would now be legal (except from the UK) because of the EEA-agreement.

Norwegian risks of BSE

If we look at the risk factors for Norway for imported BSE, I can see 2 theoretical possibilities: Waste from the 10 cattle imported from the UK between 1982 and 1986 may possibly have entered the ruminant feed chain via rendering. If any of these animals was incubating BSE and slaughtered before the 1990 ruminant feed ban, there is a risk, although the probability seems very low. There is also the possibility that dead cats fed on british petfood may have been rendered into MBM before the 1990-ban. Either way, the total quantities of contamination of our national MBM production would be very low compared to the risk-situations of most other European countries.

(During the years 1985-1990, at least 70.000 tonns of MBM and 33.000 cattle for breeding were exported from the UK to the EU. In addition there may have been millions of imported calves from the UK, for fattening, and cattle and sheep for slaughter.Waste from all these animals probably also recycled the BSE in MBM produced in the importing EU-countries).

If we consider risk factors for the emergence in Norway of an indigenous new ovine or bovine TSE (different from EU or UK-derived BSE and different from classical scrapie), this would of course be possible in any country. In such a case, recycling in ruminant feed would have stopped in 1990, and before 1990 feeding of ruminants with MBM was rather unusual. Heat treatment of rendered waste in Norway was never at low temperatures such as in the UK (however, I do not believe that 133 degrees is sufficient to destroy high levels of prion contamination - it has been suggested that we increase the temp. requirements to 135-136.) It is impossible to be sure about anything and I would not say that any country is at zero risk for emerging indigenous TSE. Today I would consider countries like the USA as highest risk, since they have not stopped feeding cattle with MBM. I would worry much more about possible BSE-related new variant scrapie in the UK, Ireland, France, Belgium, Netherlands etc... Until now, native BSE-cases have only been reported in countries where it is known that MBM from the UK has been imported. I wonder if ovine BSE might become an even more difficult problem than bovine BSE. If ovine BSE behaves like scrapie it could be spread by both vertical/maternal and horizontal transmission, and the prion could be present in much higher titres in non-nervous tissues of sheep than BSE in tissues of cattle ? Best regards,
Norwegian correspondent

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