Birth cohort of CANADIAN BSE-positive animal exported to USA

Help Support CattleToday:

flounder

Well-known member
Joined
Feb 27, 2006
Messages
1,051
Reaction score
5
Location
TEXAS
Subject: Birth cohort of CANADIAN BSE-positive animal was exported to the United States
Date: April 10, 2007 at 7:58 am PST

Beef News
Birth cohort of BSE-positive animal was exported to the United States

By John Gregerson on 4/10/2007 for Meatingplace.com


One of the birth cohorts of a Canadian bull diagnosed with bovine spongiform encephalopathy in January was exported to the United States in 2002, according to USDA's Animal and Plant Health Inspection Service.

The animal, a heifer, was sent to a Nebraska feedlot, and then was slaughtered at a Nebraska facility. APHIS indicated the animal presented a negligible risk since scientific data indicate that two BSE-positive animals rarely originate from the same herd. "Even at the height of the BSE epidemic in Britain, it was extremely rare to find a cohort at risk for the disease," APHIS spokeswoman Andrea McNally told Meatingplace.com.

APHIS spokeswoman Karen Eggerg added that the data on cohorts is based on "years of observation" rather than clinical studies, and indicated that one theory why two animals from the same herd are rarely BSE-positive is that prions, the misfolded proteins associated with BSE, generally are clumped together as a result of their sticky nature, and therefore aren't evenly distributed in feed.

After discovering the infected bull, a 79-month-old animal from Alberta, the Canadian Food Inspection Agency focused on cattle born in the same herd within 12 months. The bull became emaciated last winter and subsequently was earmarked for Canada's National BSE Surveillance Program.


http://www.meatingplace.com/MembersOnly ... item=17765




funny, i must be slipping, i did not see this on any of the usda/aphis updates.
must have another bse/base mad cow website somewhere?
i'm still waiting for official annoucnement of how safe we are from those nor98 TSE now documented in the USA too, nothing there yet either???
wonder why old ron or johanns have not come out and stated how safe we are yet from any exported mad cows from canada ???
i'm sure this is just a matter of overlook, as to we all know how USDA/APHIS et al BSE testing and reporting is done in such a timely manner, 4 to 8 months after the fact......tss


http://www.agr.state.ne.us/bse/bse.htm


TSS

ITEM 6 – BARB CASE CLUSTERS

39. Professor John Wilesmith (Defra) updated the committee on the

BSE cases born after the 1996 reinforced mammalian meat and

bone meal ban in the UK (BARB cases). Around 116 BARB cases

had been identified in Great Britain up to 22 November 2005,

mostly through active surveillance. BARB cases had decreased in

successive birth cohorts, from 44 in the 1996/1997 cohort to none

to date in the 2000/2001 cohort. However, 3 BARB cases had

been identified in the 2001/2002 cohort. Backcalculation of the

prevalence of BARB cases indicated a drop from 130 infected

animals per million (95% confidence interval 90-190) in the

1996/1997 cohort to 30 infected animals per million (95%

confidence interval 10-60) in the 1999/2000 cohort. A shift in the

geographical distribution of BSE cases, from the concentration of

pre-1996 BSE cases in Eastern England to a more uniform

14

© SEAC 2005

distribution of BARB cases, had occurred. However, it appeared

that certain post-1996 cohorts had a higher exposure to BSE in

certain areas for limited periods. Several clusters of BARB cases

within herds had been identified (5 pairs, 2 triplets and 1

quadruplet).

40. A triplet of BARB cases in South West Wales had been

investigated in detail. The triplet comprised 2 cases born in

September and October 2001 and a third in May 2002. The

animals born in 2001 were reared outdoors from the spring of 2002

but the animal born in 2002 had been reared indoors. Further

investigation of feeding practices revealed that a new feed bin for

the adult dairy herd had been installed in September 1998. In July

2002 the feed bin was emptied, but not cleaned, and relocated. All

3 BARB cases received feed from the relocated bin. This finding

suggested the hypothesis that the feed bin installed in September

1998 was filled initially with contaminated feed, that remnants of

this feed fell to the bottom of the bin during its relocation, and thus

young animals in the 2001/2002 birth cohort were exposed to

feedstuffs produced in 1998. No adult cattle had been infected

because of the reduced susceptibility to BSE with increasing age.

41. Further investigation of multiple case herds had found no

association of BARB clusters with the closure of feed mills.

42. Professor Wilesmith concluded that there is evidence of a decline

in risk of infection for successive birth cohorts of cattle. The BARB

epidemic is unlikely to be sustained by animals born after 31 July

2000. Feed bins could represent a continued source of occasional

infection and advice to farmers is being formulated to reduce this

risk. There is no evidence for an indigenous source of infection for

the BARB cases.

43. Members considered it encouraging that no other factor, apart from

feed contamination, had been identified as a possible cause of

BARB cases to date. Members commented that this study

suggests that only a small amount of contaminated feed may be

required for infection and that BSE infectivity can survive in the

environment for several years. Professor Wilesmith agreed and

noted that infection caused by small doses of infectious material

was consistent with other studies, and it would appear there is little

dilution of infectivity, if present, in the rendering system.

Additionally it appeared that the infectious agent had survived for 4

years in the feed bin.

44. The Chair thanked Professor Wilesmith for his presentation.


snip...


http://www.seac.gov.uk/minutes/final90.pdf




23.2 BSE-infected mad cows in the standing Canadian adult cattle population. very disturbing...


BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM
BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01


http://lists.ifas.ufl.edu/cgi-bin/wa.ex ... D=0&P=3854





http://lists.ifas.ufl.edu/cgi-bin/wa.ex ... T=0&P=4652





http://lists.ifas.ufl.edu/cgi-bin/wa.ex ... D=0&P=2583





Importation of Certain Commodities From BSE Minimal-risk Regions (Canada)

Environmental Assessment, October 27, 2006


http://www.aphis.usda.gov/newsroom/hot_ ... 7-2006.pdf





Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL
IMPORTS FROM CANADA


https://web01.aphis.usda.gov/BSEcom.nsf ... AutoFramed



Subject: Re: Birth cohort of CANADIAN BSE-positive animal was exported to the United States
Date: April 10, 2007 at 10:33 am PST

"It most likely" entered the food supply "given that it was slaughtered," said Karen Eggert, a spokeswoman with USDA's Animal and Plant Health Inspection Service.


"But it wouldn't have gone to slaughter if it was showing any clinical signs for BSE. We're not looking at this as a possibility that a BSE infected cow got into the United States," she said.


http://www.reuters.com/article/domestic ... 5520070410




how in the heck does she know ??? does she know what sub-clinical means ???




Date: Mon, 26 Mar 2007 15:48:11 -0600
Reply-To: Sustainable Agriculture Network Discussion Group
<[log in to unmask]>
Sender: Sustainable Agriculture Network Discussion Group
<[log in to unmask]>
From: "Terry S. Singeltary Sr." <[log in to unmask]>
Subject: Re: REPORT ON THE INVESTIGATION OF THE NINTH CASE OF BSE IN
CANADA UPDATE MARCH 26, 2007
Content-type: multipart/alternative;


Subject: Re: REPORT ON THE INVESTIGATION OF THE NINTH CASE OF BSE IN CANADA UPDATE MARCH 26, 2007
Date: March 26, 2007 at 1:29 pm PST


Attachment 1: Estimation of BSE Prevalence in Canada

snip...

Table 5 summarizes the results of the estimation of BSE prevalence in the standing Canadian adult cattle population as of August 15, 2006. Based on the expected prevalence value under the BBC model and the estimated adult herd size (Table 1), the expected number of BSE-infected animals in the standing Canadian adult cattle population is 4.1. By comparison, the expected value obtained under BSurvE Prevalence B is 3.9 per million, which corresponds to an estimated 23.2 BSE-infected animals in the standing Canadian adult cattle population.

snip...


http://www.aphis.usda.gov/newsroom/hot_ ... alence.pdf



full text ;


http://lists.ifas.ufl.edu/cgi-bin/wa.ex ... mg&P=15653




Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL
IMPORTS FROM CANADA


in my opinion this is a statement with intent to deceive and it is not
correct. There have been several cases of clinical BSE in British cattle
under 30 months and it is therefore hardly possible to think that cattle
under 30 months have virtually no risk of having BSE. In 1988 the
youngest British BSE case was 24, the second youngest 27 months old. In
1989 the youngest British BSE case was 21 and there were 4 cases only 24
months old. In 1990 there were two cases only 24 and one 26 months old.
In 1991 the youngest British BSE case was 24 and there were 3 cases only
26 months old. In 1992 the youngest British BSE case was 20!, the second
youngest 26 months old. In 1993 there was was a 29 months old case, in
1995 the UK had a 24 months old case and in 1996 one British BSE case
was 29 months old.

http://www.defra.gov.uk/animalh/bse/bse ... g-old.html



But mainly this wrong statement is misleading, because not the
clinically sick cows are the problem for consumers. The real problem are
those animals that became infected as calves and are still incubating
the infectivity during the incubation time of 5-6 years. For consumers
it is therefore totally irrelevant that cattle are at low risk to reach
the clinical stage before being 30 months old. Important for consumers
is the fact that most British BSE cases became infected as calves
(http://www.heynkes.de/peaks.htm) and that infected calves are already
amplifying the infectivity. The advantage of young calves for consumers
is that the infectivity in infected animals is low and still
concentrated around the gastro- intestinal tract. But this is not
necessarily true for bulls, which are usually slaughtered when they are
19-22 months old. They are too young to give positive results in the
actual BSE tests, but they might be infective for consumers.

For US consumers it is of no importance whether a BSE-infected Canadian
cow will show the first symptoms before or after it becomes 30 months
old. Interesting for the consumers is only

1) if cattle are infected or not,

2) where in the animal is how much of the infectivity and

3) what happens to the infectivity during slaughtering?

If the US government is really interested to reduce consumers risk, it
has to

1) stop cannibalism among farm animals (no farm animal protein and fat
in feeding stuff for farm animals, no possibility of cross contamination
of concentrate feed in mills and no lambing on pastures where scrapie
might be a problem)

2) test slaughter cattle above 24 months for BSE,

3) avoid contamination of the beef with prions from CNS by changing
slaughter methods (electrical stunning instead of captive bolt, no
immobilisation with a pithing rod, no spreading of infectivity by sawing
through the spinal cord),

4) destroy the high risk materials (brain, eyes, spinal cord, dorsal
root ganglia and other peripheral ganglia, nervous and lymphatic tissue
associated with intestine)

5) commit the whole chain from abattoir to counter in shop and
restaurant to label products from cattle and sheep, because it is only a
myth that scrapie is less infective than BSE.

In addition the US government should test all cattle and sheep which
died or had to be killed because of illness. This measure should be hold
out for at least one year in order to see the real BSE- and
scrapie-incidence in the USA....


Microbiologist Roland Heynkes

http://www.heynkes.de/default.htm



Furthermore, for the USA to continue to flagrantly ignore the findings
from Collinge/Asante et al
that BSE transmission to the 129-methionine genotype can lead to an
alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD. These
findings could have
major implications for the medical and surgical arena and human health.
this type sporadic CJD
is very prevalent in the USA ;

http://www.fda.gov/ohrms/dockets/ac/03/ ... s1_OPH.htm




snip...full text ;


https://web01.aphis.usda.gov/BSEcom.nsf ... AutoFramed



>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
From: ProMED-AHEAD
Date: Tue, 13 Oct 1998 21:59:17 -0400 (EDT)
Subject: PRO/AH> BSE - Switzerland (02)


BSE - SWITZERLAND (02)
**********************
A ProMED-mail post


In June Swiss scientists using immunological and immuno-histochemical
tests for the BSE prion found 8 cases of BSE infection among 1761
apparently healthy herd mates of Swiss cattle which had developed BSE
(a prevalence of 4.5/1000). It was then decided to test for the prion
in 3000 healthy cattle over the age of 30 months being slaughtered at
abattoirs for human consumption. In late September one infected cow
was found, a four-year-old sent for slaughter because her milk output
had fallen due apparently to mastitis. This is the first time BSE
infection has been detected in a cow that would otherwise have been
eaten, in time to take it out of the food chain.


All 3,000 have now been tested with the fast Western blot developed by
the Zurich-based firm Prionics. Of those 2,200 have also been tested
using slower immuno-histochemical methods. All the results so far
agree, including the one positive result. One possible reason for the
good agreement between tests (in the previous study different tests
agreed on only 4 of the 8 positives) is that this time, brains were
divided into hemispheres and each was sent for one test or the other.
Prion distribution seems to be laterally symmetric, so this reduced
sampling error.


The apparent prevalence of 1/3,000 is less than the 1/1,000 infected
cattle in apparently healthy herds in Switzerland calculated by Doherr
and colleagues, based on observed clinical incidence and estimated
incubation time of the disease. The discovery of only one case does
not allow the empirical calculation of a clinically significant rate.
But if the prevalence is 1/3,000, some 50 infected cattle over the age
of 30 months are being eaten per year in Switzerland.


The results of the Prionics test were available within 24 hours, which
allowed the infected carcass to be destroyed before it was sold for
meat. Swiss authorities are now considering whether to mandate testing
of all cattle at slaughter. There are fears that too many false
positives would make this prohibitively expensive, as for each case
detected the entire herd would have to be destroyed. Prionics points
out that of the 3000 tests in the current series, 2999 were negative,
indicating that while there might be false negatives, the rate of
false positives is not substantial.


Professor Picoux pointed out [ProMed 6 October] that the cow found in
the current series may not have been strictly subclinical, as she had
displayed behavioural changes which were put down, possibly
erroneously, to pain from mastitis. The early symptoms of BSE are
notoriously difficult to distinguish from other syndromes with neural
involvement. This cow possibly exemplifies the reason for much
under-reporting of BSE on the Continent: older cattle with falling
milk output or odd symptoms are simply sent for slaughter. Some of
those could have been developing BSE, but are killed before they get a
chance to develop clear symptoms.


The European Commission wants all EU countries to test cattle in
abattoirs for such hidden infection. It is to be remembered that the
levels of BSE infection expected on the Continent simply on the basis
of British cattle exports, to say nothing of the continued feeding of
meat and bone meal of questionable hygiene to livestock, are well in
excess of what has been reported. That, incidents such as the recent
surge of cases in Portugal, and the continuing, and to many people
implausible, apparent absence of BSE in Germany, suggest substantial
under-reporting.


The implications of the Swiss result for Britain, which has had the
most BSE, are complex. Only cattle aged 30 months or younger are eaten
in Britain, on the assumption, based on feeding trials, that cattle of
that age, even if they were infected as calves, have not yet
accumulated enough prions to be infectious. But the youngest cow to
develop BSE on record in Britain was 20 months old, showing some are
fast incubators. Models predict that 200-300 cattle under 30 months
per year are infected with BSE and enter the food chain currently in
Britain. Of these 3-5 could be fast incubators and carrying detectable
quantities of prion.


If one were to test cattle routinely at abattoirs in Britain, it is
possible that only those 3-5 would be detectable, and thus could be
kept out of the food chain. So routine testing may not be
cost-effective. On the other hand, these predictions are based
entirely on modelling. Some think that at least a study similar to the
Swiss one should be carried out in Britain to actually measure the
extent of infection, especially if there is a subclinical strain that
is not reflected in models based on clinical incidence.


The Swiss data do not shed light on infection before 30 months. They
did not test younger cattle as relatively few of them would be
expected to have accumulated enough prion to be detectable, so a much
larger sample size than the government was prepared to pay for
initially would have been required to detect at least one case. The
30-month cut-off was also practical (perhaps one reason it was chosen
as the limiting age in Britain) as because of dental development, the
head of a cow 30 months or older can be readily distinguished from a
younger one at the abattoir.


Whether or not screening cattle in abattoirs can make meat safe is
debated. It is claimed by some, disputed by others, that infected
cattle which have not yet accumulated detectable quantities of prion
are not infectious. So animals that test negative are safe to eat
whether infected or not. The few private Swiss butchers now using the
Prionics test to screen beef before it is marketed advertise their
wares as BSE tested, not BSE free. The efficacy of screening at
preventing the transmission of infection to people also ultimately
depends on whether detectable levels of prion in brain occur at the
same time as potentially infectious levels in muscle. That is not
known.


- --
Debora MacKenzie,
New Scientist.


<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<<

TSS
 
McNally said there was "negligible risk" from the import since scientific data shows it is rare to find another infected animal in the same herd as a BSE-positive animal.


So why have they put such an importance and spent so much time tracking down and "destroying" the birth cohorts and other animals that were in the herd... :???: Why all the hoopla about needing mandatory ID to track down BSE herd mates :???:

Kind of shows how the USDA/NCBA/CFIA "sound science", "best available science" or whatever they are calling it this week :roll: is truly the "whatever fits our argument of the day best science"... :lol: :( :mad:

What a farce these Corporate bought government "prostitute scientists" are.... :mad: :mad:
 
Hey,oldtimer, we have some of the best scientists money can buy. What more do you want :D
 
Hindsight is 20/20, but before we knew we had BSE in CANADA we exported some animals from the same herd to the US. But we can trace one heifer exported to the US back in 02.
That is why you guys need a national ID program so you can do accurate traceouts forget a bse positive animals what about FAM disease. What happens if and when foot and mouth comes into the US from banana republic beef. It would be crucial to have a tracking system to gain control of the disease. That is why the hoopla around a tracking system!
 

Latest posts

Top