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From: TSS ()
Subject: Re: Mad cow disease case found in Austria -ministry
Date: June 21, 2005 at 9:33 pm PST

In Reply to: Mad cow disease case found in Austria -ministry posted by TSS on June 21, 2005 at 9:10 am:

Austria Finds Second Case of Mad Cow Disease


AUSTRIA: June 22, 2005

VIENNA - A case of mad cow disease has been found in Austria, the second in the Alpine country's history, the health and agriculture ministers said on Tuesday.

The ministers called a snap news conference to announce the case of the deadly brain-wasting disorder, or bovine spongiform encephalopathy (BSE).
"The reason for this short-notice press conference today is the confirmation of a case of BSE in an Austrian cow," Health Minister Maria Rauch-Kallat told reporters.

Mad cow disease was first identified in Britain in 1986.

Scientists say there is a strong link between humans eating tainted meat and the the risk of catching the disease. More than 100 people have died so far in Europe from the human form of mad cow disease, mostly in Britain.

The disease was found during a routine test on an 11-year-old cow from a small farm of seven cattle near the German border in the western province of Vorarlberg. All seven animals were slaughtered and cremated.

Agriculture Minister Josef Proell said it was a standard safety procedure in Austria for cattle older than 24 months that die of unknown causes to be tested for BSE.

As this cow died unexpectedly in late May after showing suspicious signs including tiredness, it was tested.

How the animal became infected was not clear, said Josef Koefer, divisional head at Austrian food safety agency AGES.

"The normal route is via the feed. The other variant that I am considering is a spontaneous mutation in the prions," he said.

BSE is caused by abnormal or misfolded prion proteins in an animal's brain.

"We may never know for certain," Koefer added.

Feeding animal meal to farm animals has been banned in Austria since 1991.

The European Union tightened food safety laws after a BSE scare in the 1990s. It has banned the use of animal parts in feed and also removed high-risk material such as spinal cord, intestines and brain from the food and feed chain.

Austria's first case of BSE was found in December 2001.

Austria's Proell said this showed Austrian cattle were screened properly.

"The system works. Consumers can be assured that Austrian beef is safe," he told reporters.

"Compared with all other European countries, we are absolutely among the best," Proell said.

"Germany currently has had 356 BSE cases, Switzerland ... has had 456 BSE cases. Austria, with Luxembourg, leads Europe with the second BSE case," he added.

(Additional reporting by Francois Murphy and Alexandra Schwarz)

Story by Marcus Kabel


>>>"The normal route is via the feed. The other variant that I am considering is a spontaneous mutation in the prions," he said. <<<<

seems everyone is getting on this spontaneous banwagon, when they cannot or will not explain the real routes and sources.

i dont buy it. everyone that believes in this fairy tail, including some at USDA et al, seems to believe spontaneous BSE arises in roughly 1 - 3 cases out of every one million head of cattle. IF this is the case, then how come they have not had a case since 2001. the head count in 1997 was 2.163 million head. in 1987 it was 2.59 million head. SO, if you go with the fairy tail spontaneous theory, they should have documented many more head of BSE mad cows. but they did not. so, if this spontaneous theory is correct, where are the other mad cows? IS Austria's BSE surveillance that bad?

Final report on the updated

assessment of the

Geographical BSE-Risk

(GBR) of

AUSTRIA - 2002

Provided to the SSC on 16 May 2002


Independent experts have produced this report, applying an innovative

methodology by a complex process to data that were supplied by the

responsible country authorities. Both, the methodology and the

process, are described in detail in the final opinion of the SSC on "the

Geographical Risk of Bovine Spongiform Encephalopathy (GBR)",

6 July 2000 and its update of 11 January 2002. These opinions are

available at the following Internet address:

This report, and the opinion of the SSC based on it, is now serving as

the risk assessment required by the TSE-Regulation EU/999/2001 for

the categorisation of countries with regard to their BSE-status. The

final BSE-status categorisation depends also on other conditions as

stipulated in annex II to that TSE-Regulation.


If true would result in mean of 2 cases per year and <100 cattle oral ID50s to humans over 20 years

Test in absence of feed ban casts some doubt of plausibility of this hypothesis


If transmission possible (no American scrapie can infect cattle) predict mean of 2 BSE cases/yr

<100 cattle oral ID50s to humans over 20 years

Harvard Center for Risk Analysis

- 1 -

Evaluation of the Potential for Bovine Spongiform

Encephalopathy in the United States

Joshua T. Cohen

Keith Duggar

George M. Gray

Silvia Kreindel

Harvard Center for Risk Analysis

Harvard School of Public Health

Hatim Abdelrahman

Tsegaye HabteMariam

David Oryang

Berhanu Tameru

Center for Computational Epidemiology

College of Veterinary Medicine

Tuskegee University

November 26, 2001


- 19 -

2.3.1 Spontaneous BSE

A potential way in which BSE could be introduced into the United States is the

development of a spontaneous case of a BSE in a native animal. A "spontaneous case" is one that

occurs in an animal with no known risk factors for development of BSE. The presumed

mechanism by which a BSE could occur spontaneously is by the mutation of the PrP gene to a

Section 2

- 20 -

form that codes for PrPsc, and subsequent recruitment of PrPc until disease is manifest (Prusiner,

1989); (for review see: (Chesebro, 1999). There is no direct evidence of this mechanism,

although some argue that all mammals might have a low spontaneous rate of TSE (Hueston,

1997). In addition, a transgenic animal over-expressing the PrP gene has apparently replicated

the human TSE GSS (Hsiao et al., 1991). Recent results, in which mice expressing the same

point mutation but at normal levels failed to develop disease (Manson et al., 1999), suggest the

mutations may increase susceptibility rather than directly cause the disease. Although at this time

there is no scientific evidence suggesting that spontaneous BSE exists, the BSE Inquiry suggested

that TSEs could possibly develop sporadically in other species, as they do in humans (BSE

Inquiry, 2000). In contrast, the Review of the origin of BSE (Horn et al., 2001) concluded that

although the spontaneous case hypothesis cannot be excluded, there is no evidence supporting the

presence of sporadic form prion disease in cattle or sheep.

It is not possible to determine for any particular TSE whether the original cause was a

mutation or transmission of disease from another species or from the same species. For example,

transmissible mink encephalopathy (TME) has no known origin. There are a number of theories,

most of which focus on transmission from another species (Marsh et al., 1991). In the case of

BSE, there is little evidence from the epidemiology to suggest that cases arise without some

exposure to infectivity (Wilesmith et al., 1991, Kimberlin and Wilesmith, 1994, Horn et al.,

2001). On the other hand, there are a small number of cases for which there are no known risk

factors (MAFF born after the ban, 2000 (MAFF, 2000a); Denmark born after the ban, 2000

(Tegtmeier et al., 2001)).

The existence of a spontaneous form of TSEs in animals is controversial. In humans,

cases of CJD in persons with no known risk factors or exposure to the disease occur at an annual

incidence of approximately one per million. The incidence appears to be relatively constant

around the world, regardless of diet, environment, or other factors that may hypothetically

influence disease rates. Cases in individuals with no known risk factors are often referred to as

"sporadic CJD." The etiology of sporadic CJD is unknown. Sporadic CJD appears almost

exclusively in humans more than 50 years old. Cases appear to occur without a predictable

epidemiological pattern (Brown et al., 1994b, Will et al., 1986). Sporadic CJD accounts for 85%

of all cases and these cases are characterized by a relatively rapidly progressive clinical course,

although rare variants have shown an extensive duration of clinical illness (Brown et al., 1984).

It is sometimes asserted that the rate of sporadic CJD in humans is likely to be representative of

Section 2

the rate of spontaneous BSE in cattle (Biopharm, 1997), although the rate in cattle has never been

directly measured and may in fact be zero.

2.3.2 Importation of BSE Infectivity into the United States

This section describes the potential for the importation of BSE infectivity into the United

States, including the importation of live cattle (Section and feed material (Section Importation of Live Cattle from the UK

The U.S. imported animals from the UK during the BSE epidemic. Between January 1,

1981, and July 1989, the United States imported 334 cattle from the UK. Ninety-six percent of

these animals were beef breeding stock, while the remaining four percent were dairy cattle. In

1989, the US prohibited the importation of ruminants from countries affected with BSE.

Of the 334 UK imports, 161 were disposed of in a manner that eliminates the possibility

that they could have contaminated either human food or animal feed. The remaining 173 cattle

were imported before the peak of the epidemic, and none came from a birth cohort in which a

BSE case is known to have developed (SSC, 2000d). Of these 173, 164 (94.8%) were beef

breeding animals and nine (5.2 %) were dairy animals. It is possible that remains from some of

the 173 cattle imported from the UK between 1980 and 1989 could have ended up in either

animal feed, human food, or both. Section 3.4.3 describes our risk assessment of this scenario.


The study apparently treats the scrapie transmission (Section 2.3.3,
Page 23) and the spontaneous BSE case (Section 2.3.1, Page 21) at
the same level as the above listed priority routes. Below we provide
an example of this inconsistency with what is considered major

HERE, we have Dr. Dehaven, this is a hoot. he claims there is PROOF of a spontaneous CJD, but seems sure there is NO proof of spontaneous BSE. i would like ron to show me this PROOF he has on a spontaneous CJD. how can you have one and not the other?

As far as spontaneous cases, that is a very difficult issue. There is no evidence to prove that spontaneous BSE occurs in cattle; but here again it's an issue of proving a negative. We do know that CJD, the human version of the disease, does occur spontaneously in humans at the rate of about 1 in 1 million. We don't have enough data to definitively say that spontaneous cases of BSE in cattle occur or do not occur.

“Again, it's a very difficult situation to prove a negative.

“So a lot of research is ongoing. Certainly if we do come up with any positive samples in the course of this surveillance we will be looking at that question in evaluating those samples but no scientifically hard evidence to confirm or refute whether or not spontaneous cases of BSE occur.!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retrievecontent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/_th/J_2_9D/_s.7_0_A/7_0_1OB%3FPC_7_2_5JM_contentid%3D2004%252F03%252F0106.html+spontaneous+BSE&hl=en

PLUS, Prusiner the prion man himself that is so gung ho for this spontaneous theory$, he himself said that his spontaneous TSE he developed in the lab, did NOT look like any other TSE pathologically. ...


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