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From: TSS ()
Subject: Experimental Transmission of Transmissible Mink Encephalopathy (Tme) to Cattle by Intracerebral Inoculation
Date: October 27, 2006 at 1:08 pm PST

Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: Experimental Transmission of Transmissible Mink Encephalopathy (Tme) to Cattle by Intracerebral Inoculation


Hamir, Amirali
Kunkle, Robert
Miller, Janice - ARS RETIRED
Greenlee, Justin
Richt, Juergen

Submitted to: International Veterinary Vaccines and Diagnostics Conference
Publication Type: Abstract
Publication Acceptance Date: March 15, 2006
Publication Date: June 25, 2006
Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Greenlee, J.J., Richt, J.A. 2006. Experimental transmission of transmissible mink encephalopathy (TME) to cattle by intracerebral inoculation [abstract]. 4th International Veterinary Vaccines and Diagnostics Conference. p. 89. Paper No. PO53.

Technical Abstract: To compare clinicopathological findings of transmissible mink encephalopathy (TME) with other transmissible spongiform encephalopathies (TSE, prion diseases) that have been shown to be experimentally transmissible to cattle (sheep scrapie, and chronic wasting disease, CWD), 2 groups of calves (n = 4 each) were intracerebrally inoculated with TME agents from 2 different sources (mink with TME and a bovine with TME). Two uninoculated calves served as controls. Within 15.3 months post inoculation (PI), all animals from both inoculated groups developed clinical signs of central nervous system (CNS) abnormality; their CNS tissues had microscopic spongiform encephalopathy (SE); and PrP**res was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify TME PrP**res but also develop clinical CNS signs and extensive lesions of SE. The latter has not been shown with other TSE agents (scrapie and CWD) similarly inoculated into cattle. The findings also suggest that the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) would detect TME in cattle should it occur naturally. However, it would be a diagnostic challenge to differentiate TME in cattle from BSE. Our recent preliminary results indicate that WB may be able to differentiate between bovine TME and BSE.

To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

•Department of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in


Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough
and Burger who demonstrated that the disease was transmissible with a long incubation
period, and that affected mink had a spongiform encephalopathy similar to that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965).
Because of the similarity between TME and scrapie, and the subsequent finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was
concluded that TME most likely resulted from feeding mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time provided
evidence that they may be different. Epidemiologic studies on previous incidences of
TME indicated that the incubation periods in field cases were between six months and
one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be
transmitted to mink in less than one year.
To investigate the possibility that TME may be caused by a (particular strain of
scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie
agent, including their sheep or goat sources, were inoculated into a total of 61 mink.
Only one mink developed a progressive neurologic disease after an incubation period of
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused
by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent
from an unidentified source.


A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were "acting funny", and some had died. At this time, we
visited the farm and found that approximately 10% of all adult mink were showing
typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over
their _backs like squirrels. These signs were followed by progressive deterioration of
neurologic function beginning with locomoior incoordination, long periods of somnolence
in which the affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over the past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy
cattle and a few horses. Sheep had never been fed.

Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after incubation
periods of four months. To investigate the possible involvement of cattle in this disease
cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally
with a brain suspension from affected mink. Each developed a fatal spongiform
encephalopathy after incubation periods of 18 and 19 months.

These findings suggest that TME may result from feeding mink infected cattle and
we have alerted bovine practitioners that there may exist an as yet unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new
bovine spongiform encephalopathy has recently been reported in England (Wells et al.,
1987), and investigators are presently studying its transmissibility and possible
relationship to scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be
confused with rabies in the United Stales and not be diagnosed. Presently, brains from
cattle in the United States which are suspected of rabies infection are only tested with
anti-rabies virus antibody and are not examined histopathologically for lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no agent-
specific proteins or nucleic acids identified for these transmissible neuropathogens, one
means of distinguishing them is by animal passage and selection of the biotype which
grows best in a particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral
backpassage of the experimental bovine agent resulted in incubations of only four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine passage.
Mink fed infected bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.

These studies were supported by the College of Agricultural and Life Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United
States Department of Agriculture. The authors also wish to acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.

Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.


Date: July 15, 2006 at 5:52 am PST

Pelt Production Up 3 Percent

Mink pelt production in the United States in 2005 totaled
2.63 million pelts, up 3 percent from 2004. Wisconsin, the largest
mink producing State, produced 778,000 pelts. Utah the second
largest producing State, produced 600,000 pelts.

The number of pelts by color class as a percent of the total U.S.
production in 2005 is as follows: Black at 47.6 percent, Mahogany
at 20.9 percent, Blue Iris at 11.3 percent, Demi/Wild at
6.3 percent, Sapphire at 4.0 percent, and White at 3.8 percent.
The remaining color classes accounted for 6.1 percent.

Value of Pelt Production Up 33 Percent

Mink pelts produced during the 2005 crop year were valued at
$160 million, up 33 percent from $120 million a year ago. The
average price per pelt for the 2005 crop year was $60.90, up from
$47.10 in 2004. .....snip.......end


3.9.11 Mink Producers

Mink offal is now rendered with other species and will decline in value under the first four

regulatory options.


Mink are raised for their pelts and oil. Most mink farmers kill and pelt their own animals

once a year near the end of November or in early December. Once the pelts are removed, the fat is

then scrapped from the hide. This fat is used to manufacture mink oil that is sought for cosmetic

uses because of its hypoallergenic qualities and in leather treatments. The total value of mink

production in 1995 was $143 million, an increase of 72 percent from 1994.

In 1995, 446 mink farms produced a total of 2.69 million pelts (NASS, 1996b). Mink

producers vary in size but most are small operations. Mink farming is concentrated in Utah (130


farms), Wisconsin (77 farms), and Minnesota (52 farms). There has been recent consolidation

within the industry, with the number of farms decreasing by 8 percent from 1993 to 1994 and 3

percent from 1994 to 1995. The market price for mink pelts is subject to wide demand fluctuations

based on fashion and weather.

Once the pelt and fat are removed, the entire carcass is then rendered. Mink carcasses sent

to rendering (minus the pelt and fat) weigh an average of 2.5 pounds, so the total estimated offal

produced per year is 6.7 million pounds. Mink farmers are reported to have difficulty with getting

renderers to pick-up their material because of its low volume and the infrequency of offal


WHAT sort of TME surveillance program is in place now, if any???

DO they test for TSE in Mink and what are these figures if so ???



AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.


Feline Spongiform Encephalopathy (FSE)
FSE was first identified in Britain in 1990. Since then there have been 87 cases in Great Britain, one in Northern Ireland, one in Norway and one in Liechtenstein. FSE is not an easy disease to study. Although Britain has a large cat population they would not normally have been subjected to close neurological examination in the past. Nevertheless, sufficient numbers of FSE cases have been seen and investigated to permit an association with BSE to be made. Obtaining lifetime feeding history for cats is not easy, so although all have eaten foods that would be expected to contain specified bovine offals, no particular type of food can be implicated.

The epidemic in cats is often thought to be a useful model for past human exposure to BSE. The number of feline cases has declined dramatically.

As Defra has not historically held responsibility for investigating disease, other than rabies, in domestic pets, most of the information gathered about FSE in domestic cats and zoo animals has been provided through the good will of owners and veterinary practitioners. Laboratory diagnosis of a spongiform encephalopathy in any species has however been notifiable since November 1994, thus ensuring that cases would not be missed.

Interestingly, when brain tissue from some of the early cats identified as having FSE, was inoculated into mice, the pattern of incubation periods and lesion profiles in the mice was indistinguishable from that produced by BSE.

In exotic cats there have now been nine cases in cheetahs (three were diagnosed abroad but originated in Britain), three in pumas, three in ocelots, two in tigers and two in lions.

In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.


Zanusso-G, Nardelli-E Rosati-A Fabrizi-G-M Ferrari-S Carteri-A Desimone-F Rizutto-N Monaco-S. Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy. LANCET, 1998 V352, N9134, OCT 3, Pp 1116-1117.

Pearson G. R. et al. 1992. Feline spongiform encephalopathy: fibril and PrP studies. Veterinary Record. 131. 307-310.

Wyatt. J. M. et al. 1991. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.

Gruffydd-Jones T. J. et al. 1991. Feline spongiform encephalopathy. J. Small Animal Practice. 33. 471-476.

Willoughby K. 1992. Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record. 131. 431-434.

Image] Research letters Volume 352, Number 9134 [Image] 3 October
[Previous] [Next]

[Image][Image]Simultaneous occurrence of spongiform encephalopathy in a man
and his cat in Italy

Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, Sergio
Ferrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, Salvatore

Transmissible spongiform encephalopathies (TSE) encompass inherited,
acquired, and sporadic mammalian neurological disorders, and are
characterised by the conversion of the cellular prion protein (PrP) in an
insoluble and protease-resistant isoform (PrPres). In human TSE, four types
of PrPres have been identified according to size and glycoform ratios, which
may represent different prion strains. Type-1 and type-2 PrPres are
associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with
iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that
variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prion
strain.2-4 The BSE strain has been identified in three cats with feline
spongiform encephalopathy (FSE), a prion disease which appeared in 1990 in
the UK.5 We report the simultaneous occurrence of sporadic CJD in a man and
a new variety of FSE in his cat.

A 60-year-old man, with no unusual dietary habits, was admitted in November,
1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, and
myoclonus. An electroencephalogram (EEG) showed diffuse theta-delta
activity. A brain magnetic resonance imaging scan was unremarkable. 10 days
later, he was speechless and able to follow only simple commands. Repeat
EEGs showed periodic triphasic complexes. 2 weeks after admission, he was
mute, akinetic, and unable to swallow. He died in early January, 1994.

His 7-year-old, neutered, female shorthaired cat presented in November,
1993, with episodes of frenzy, twitching of its body, and hyperaesthesia.
The cat was usually fed on canned food and slept on its owner's bed. No
bites from the cat were recalled. In the next few days, the cat became
ataxic, with hindquarter locomotor dysfunction; the ataxia got worse and
there was diffuse myoclonus. The cat was killed in mid-January, 1994.

No pathogenic mutations in the patient's PrP gene were found. The patient
and the cat were methionine homozygous at codon 129. Histology of the
patient's brain showed neocortical and cerebellar neuronal loss,
astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed a
punctate pattern and paralleled spongiform changes (figure B). The cat's
brain showed mild and focal spongiosis in deeper cortical layers of all four
lobes (figure C), vacuolated cortical neurons (figure D), and mild
astrogliosis. The cerebellar cortex and the dentate nucleus were gliosed.
Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, and
caudate nucleus (figure E). Western blot analysis of control and affected
human and cat brain homogenates showed 3 PrP bands of 27-35 kDa. After
digestion with proteinase K and deglycosylation, only samples from the
affected patient and cat showed type-1 PrPres, with PrP glycoform ratios
comparable to those observed in sporadic CJD1 (details available from


Microscopic sections of patient and cat brains

A: Occipital cortex of the patient showing moderate spongiform
degeneration and neuronal loss (haematoxylin and eosin) and B: punctate
perineuronal pattern of PrP immunoreactivity; peroxidase
immunohistochemistry with monoclonal antibody 3F4. C: cat parietal cortex
showing mild spongiform degeneration (haematoxylin and eosin).D:
vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidase
immunohistochemistry with antibody 3F4 shows punctate perineuronal
deposition of PrP in temporal cortex.

This study shows a spatio-temporal association between human and feline
prion diseases. The clinical features of the cat were different from
previously reported cases of FSE which were characterised by gradual onset
of behavioural changes preceding locomotor dysfunction and ataxia.5
Neuropathological changes were also at variance with the diffuse spongiosis
and vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern of
PrP deposition, similar in the cat and in the patient, was atypical for a
BSE-related condition. Evidence of a new type of FSE was further provided by
the detection of a type-1 PrPres, other than the BSE-associated type 4.2
Taken together, our data suggest that the same agent strain of sporadic CJD
was involved in the patient and in his cat.

It is unknown whether these TSE occurred as the result of horizontal
transmission in either direction, infection from an unknown common source,
or the chance occurrence of two sporadic forms.

1 Parchi P, Castellani R, Capellari S, et al. Molecular basis of phenotypic
variablity in sporadic Creutzfeldt-Jakob disease. Ann Neurol 1996; 39:
767-78 [PubMed].

2 Collinge J, Sidle KCL, Meads J, Ironside J, Hill AF. Molecular analysis of
prion strain variation and the aetiology of 'new variant' CJD. Nature 1996;
383: 685-90 [PubMed].

3 Bruce ME, Will RG, Ironside JW, et al. Transmissions to mice indicate that
'new variant' CJD is caused by the BSE agent. Nature 1997; 389: 498-501

4 Hill AF, Desbruslais M, Joiner S, et al. The same prion strain causes vCJD
and BSE. Nature 1997; 389: 448-50 [PubMed].

5 Pearson GR, Wyatt JM, Henderson JP, Gruffydd-Jones TJ. Feline spongiform
encephalopathy: a review. Vet Annual 1993; 33: 1-10.

Sezione di Neurologie Clinica, Dipartimento di Scienze Neurologiche e della
Visione, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy
(S Monaco; e mail; and Istituto Zooprofilattico
Sperimentale della Lombardia e dell' Emilia, Brescia



worse still, there is serious risk the media could get
to hear of such a meeting...


Crushed heads (which inevitably involve brain and spinal cord material)
are used to a limited extent but will also form one of the constituent
raw materials of meat and bone meal, which is used extensively in
pet food manufacturer...

2. The Parliamentary Secretary said that he was concerned
about the possibility that countries in which BSE had not
yet been detected could be exporting raw meat materials
(in particular crushed heads) contaminated with the disease
to the UK for use in petfood manufacture...


YOU explained that imported crushed heads were extensively used in the
petfood industry...

In particular I do not believe one can say that the levels of
the scrapie agent in pet food are so low that domestic animals are
not exposed...

some 100+ _documented_ TSE cats of all types later...tss

on occassions, materials obtained from slaughterhouses
will be derived from sheep affected with scrapie or
cattle that may be incubating BSE for use in petfood manufacture...

Meldrum's notes on pet foods and materials used


Confidential BSE and __________________

1st case natural FSE

FSE and pharmaceuticals

confidential cats/dogs and unsatisfactory posture
MAFFs failure to assure key research

38. When Mr Gummer, Mr Meldrum, Mrs Attridge (MAFF) and Dr Pickles gave evidence to the
Agriculture Select Committee on 23 May 1990, the following exchange took place:

‘(Mr Martlew) Minister, you are well aware there is a considerable degree of concern amongst pet owners in the country
with regard to the safety of their domestic animals, especially cats and dogs. I wonder if you could give me an update on the
situation? I wonder if you could tell the Committee how many dead cats are actually suspected of dying of the equivalent of
BSE and whether any tests are being carried out at the moment on dogs?

(Mr Gummer) Well, there are two confirmed cases of cats who have died of encephalopathy and one which is being
investigated at this moment. [I] have announced that information already, I have no further information at this point, although
some newspapers have suggested some other things I have to tell you that is the information I have got. As you know I
published the results of the first cat investigation and I shall publish these results, as I said, once they are confirmed generally.
There is a real problem about these encephalopathy, we know that cats are susceptible to encephalopathy, you can
experimentally show that, but what you cannot tell is whether they have always had encephalopathies. This is a difficult
issue. We do know that cats have been found to have diseases, everybody has then rushed about saying: ‘Gosh, there is this
new disease’ and then later it has been discovered that in fact the cats have, as far as we know, always had that disease. Of
course, cats are not normally investigated. Dead cats, if I may say so, are not very often post-mortemed, if that is the right
word. I questioned this advice because I said: ‘What about a cat suspected of rabies, would you not pick it up while you
were doing the rabies?’ and I am told the mechanism for looking at a rabid cat is such that you would not necessarily, indeed
you would be unlikely to find the encephalopathy you now find when you are looking for it. Indeed, each of the three cats
that have so far been either suspected or confirmed of having an encephalopathy were only suspected because of the
arguments about BSE and because we asked vets to look out for these things in any case, certainly after the first one. The
vet who found the first one said that he was drawn to it by thinking of what he had seen on the television and the rest of it.
We are in the difficulty of first not knowing whether cats have always had this and, therefore, that we caught not to be looking
for some sort of new cause of it. Secondly, there is certainly no evidence whatsoever that it is connected with feed. Thirdly,
I must say the connection with feed is difficult to see at this moment because of the home background of the different cats
whose feeding habits are very different indeed and the fact that the feed industry has taken as to 95 per cent of its members,
and probably very much nearer 100 per cent because the smaller firms have followed that advice, particular measures to
protect its feed from any possible contamination. I find it very difficult to say other than we have had these cases, that the
reason that we have had these cases is largely because of the concern about BSE but there is absolutely no evidence at all
that it is connected with BSE and may be another line of these things, like other separate lines, and we shall have to find

39. An annex to a memorandum submitted to the Agriculture Select Committee in May 1990 by Professor
Richard Lacey and Dr Stephen Dealler includes the following:

‘Cats appear to be now at risk of a spongiform encephalopathy (possibly to be called feline spongiform encephalopathy).
This was not recorded before the appearance of BSE and sheep offal had been fed to cats from any years. It would be
likely that FSE and BSE are linked in some way. Prospective and retrospective controlled (if possible) studies should take
place in which cats fed with scrapie and BSE infected meat should be examined using histopathological and PrP isolation
techniques to test for infection. These experiments should be funded and organised independently from the food, animal
food, or farming industries and the Government. Carnivores were not previously thought to be at risk of catching a prion
encephalopathy by mouth and this was thought to be reasonable because of Darwinian selection theory. If cats were found
to be at risk of catching FSE from cattle then this would confirm that BSE has a different infective spectrum from scrapie; a
very serious finding.’[45]

40. When Sir Richard Southwood gave oral evidence to the Agriculture Select Committee, he said:

‘The case of the cat is the first case of spongiform encephalopathy ever in a cat. Well, it appears to be – but if poor moggie
got a bit of the staggers, you took it along to the vet and said it was not very happy, it would be put to sleep in the past and
no one would have paid £300 to have a post mortem undertaken. So it is just possible that these were occurring before and
were in fact caught from moggie being fed scrapie offal from sheep. I cannot say.’[46]

NEXT, ask yourself how many cats and dogs have ever been tested for TSE in the USA ???

Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: Identification and Characterization of U.S. Bse Cases


Richt, Juergen

Submitted to: Meeting Abstract
Publication Type: Abstract
Publication Acceptance Date: April 25, 2006
Publication Date: May 28, 2006
Citation: Hall, S.M., Richt, J., Davis, A., Kluge, J., Simmons, M., Stack, M., Spencer, Y. 2006. Identification and characterization of U.S. BSE cases [abstract]. Prion Diseases of Domestic Livestock. p. 25.

Technical Abstract: Bovine Spongiform Encephalopathy (BSE) surveillance has been ongoing in the USA since the early 1990¿s and initial testing was done at the USDA, National Veterinary Services Laboratories (NVSL) utilizing routine histopathology exclusively. In 1995, the immunohistochemistry (IHC) test was incorporated into surveillance testing in addition to routine histopathology. By 1999 virtually all BSE screening was performed by IHC and by 2001 the NVSL had switched to an automated IHC procedure. In 2002 and 2003 the NVSL tested about 20,000 high risk animals each year by IHC. In December, 2003 an animal was identified by IHC as positive for BSE (Case 1); this animal was determined to be imported from Canada. After this animal was identified, in June 2004 the USDA began its enhanced surveillance program as a shared effort between selected state veterinary diagnostic laboratories and NVSL, as part of the National Animal Health Laboratory Network. The plan called for testing as many targeted high risk animals as possible in a 12-18 month period. From June 1, 2004 through March 21, 2006, over 650,000 animals have been tested (Bio-Rad ELISA). Of those tested, two animals (Cases 2 and 3) have been identified as positive for BSE. While all three cases were strongly positive by Bio-Rad ELISA, Cases 2 and 3 have common features which are distinct from Case 1. Definitive spongiform changes in the obex, strong immunohistochemical reactions, and Western blot patterns similar to European BSE cases were observed in Case 1. In contrast, Cases 2 and 3 did not contain definitive histological lesions of BSE and the IHC staining was less intense than Case 1. In addition, Cases 2 (approximately 12 years) and Case 3 (approximately ten years) were older animals while Case 1 was 6.5 years old. Western blot analysis, PrP**Sc from Case 1 showed molecular features similar to typical BSE isolates, whereas PrP**Sc from Cases 2 and 3 revealed an unusual molecular PrP**Sc pattern: molecular mass of the unglycosylated and monoglycosylated isoform was higher than that of typical BSE isolates. Case 1 contained more PrP**Sc per brain tissue mg equivalent compared with Cases 2 and 3 using antibody 6H4. In Western Blot analysis, Case 2 and Case 3 were strongly positive with antibody P4, while Case 1 was negative or weakly positive with P4.

>> Differences in tissue distribution could require new regulations >> regarding specific risk material (SRM) removal.


full text 33 PAGES ;

It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.


Office Note


A The Present Position with respect to Scrapie
A] The Problem

Scrapie is a natural disease of sheep and goats. It is a slow
and inexorably progressive degenerative disorder of the nervous system
and it ia fatal. It is enzootic in the United Kingdom but not in all

The field problem has been reviewed by a MAFF working group
(ARC 35/77). It is difficult to assess the incidence in Britain for
a variety of reasons but the disease causes serious financial loss;
it is estimated that it cost Swaledale breeders alone $l.7 M during
the five years 1971-1975. A further inestimable loss arises from the
closure of certain export markets, in particular those of the United
States, to British sheep.

It is clear that scrapie in sheep is important commercially and
for that reason alone effective measures to control it should be
devised as quickly as possible.

Recently the question has again been brought up as to whether
scrapie is transmissible to man. This has followed reports that the
disease has been transmitted to primates. One particularly lurid
speculation (Gajdusek 1977) conjectures that the agents of scrapie,
kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of
mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed
for human or animal food at slaughter or rendering plants" (ARC 84/77)"
The problem is emphasised by the finding that some strains of scrapie
produce lesions identical to the once which characterise the human

Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety
of laboratory personnel requires prompt attention. Second, action
such as the "scorched meat" policy of USDA makes the solution of the
acrapie problem urgent if the sheep industry is not to suffer



Date: February 12, 2006 at 1:03 pm PST


Chair: Dr. Jim Logan, Cheyenne, WY

Vice Chair: Dr. Joe D. Ross, Sonora, TX

Dr. Deborah L. Brennan, MS; Dr. Beth Carlson, ND; Dr. John R. Clifford, DC; Dr. Thomas F. Conner, OH; Dr. Walter E. Cook, WY; Dr. Wayne E. Cunningham, CO; Dr. Jerry W. Diemer, TX; Dr. Anita J. Edmondson, CA; Dr. Dee Ellis, TX; Dr. Lisa A. Ferguson, MD; Dr. Keith R. Forbes, NY; Dr. R. David Glauer, OH; Dr. James R. Grady, CO; Dr. William L. Hartmann, MN; Dr. Carolyn Inch, CAN; Dr. Susan J. Keller, ND; Dr. Allen M. Knowles, TN; Dr. Thomas F. Linfield, MT; Dr. Michael R. Marshall, UT; Dr. Cheryl A. Miller, In; Dr. Brian V. Noland, CO; Dr. Charles Palmer, CA; Dr. Kristine R. Petrini, MN; Mr. Stan Potratz, IA; Mr. Paul E. Rodgers, CO; Dr. Joan D. Rowe, CA; Dr. Pamela L. Smith, IA; Dr. Diane L. Sutton, MD; Dr. Lynn Anne Tesar, SD; Dr. Delwin D. Wilmot, NE; Dr. Nora E. Wineland, CO; Dr. Cindy B. Wolf, MN.

The Committee met on November 9, 2005, from 8:00am until 11:55am, Hershey Lodge and Convention Center, Hershey, Pennsylvania. The meeting was called to order by Dr. Jim Logan, chair, with vice chairman Dr. Joe D. Ross attending. There were 74 people in attendance.

The Scrapie Program Update was provided by Dr. Diane Sutton, National Scrapie Program Coordinator, United States Department of Agriculture (USDA), Animal and Plant Health Inspection Services (APHIS), Veterinary Services (VS). The complete text of the Status Report is included in these Proceedings.

Dr. Patricia Meinhardt, USDA-APHIS-VS-National Veterinary Services Laboratory (NVSL) gave the Update on Genotyping Labs and Discrepancies in Results. NVSL conducts investigations into discrepancies on genotype testing results associated with the Scrapie Eradication Program. It is the policy of the Program to conduct a second genotype test at a second laboratory on certain individual animals. Occasionally, there are discrepancies in those results. The NVSL conducts follow-up on these situations through additional testing on additional samples from the field and archive samples from the testing laboratories.

For the period of time from January 1, 2005, until October 15, 2005, there were 23 instances of discrepancies in results from 35 flocks. Of those 23 instances, 14 were caused by laboratory error (paperwork or sample mix-up), 3 results from field error, 5 were not completely resolved, and 1 originated from the use of a non-approved laboratory for the first test. As a result of inconsistencies, one laboratory’s certification was revoked by APHIS-VS.

To reduce/eliminate these problems, the Program has placed additional quality requirements on the testing laboratories: additional review of final reports, additional coding systems for testing operations, strict follow-up and reports to NVSL on corrective actions, dual data entry systems, and more frequent inspections.

The Agricultural Research Services (ARS) Scrapie Research Update was given by Janet Alverson, USDA- ARS. Dr. Alverson reported on the effect of multiple births and fetal position within the uterus on PrP-Sc accumulation in fetal cotyledons. Fetal cotyledons of fetuses with

resistant genotypes can accumulate PrP-Sc when positioned next to a fetus of susceptible genotype with cotyledons positive for PrP-Sc accumulation.

Scrapie Surveillance Evaluation Working Group Update was presented by Tracey Lynn, Epidemiologist with the National Surveillance Unit, Center for Epidemiology and Animal Health (CEAH). The presentation provided a background on evaluation, a quick review of analyses completed to date by the scrapie surveillance evaluation working group, and some of the preliminary findings. The process of surveillance system evaluation is undertaken to assist a disease control program with identifying possible improvements to their surveillance system, and includes an assessment of the overall utility of the system, identification of potential gaps in coverage, and an evaluation of the overall performance of the system. The scrapie surveillance evaluation working group reviewed the structure and processes of the scrapie surveillance program, as well as various quality and effectiveness measures.

Overall, 98-99% of surveillance samples come from the Regulatory Scrapie Surveillance System (RSSS), so the RSSS system has been the primary focus of the evaluation process. The working group developed a flow chart indicating the flow of sheep through RSSS, which identified potential gaps in surveillance coverage, including custom kill plants and sheep being exported to Mexico. Spatial analyses can assist in identifying areas with high density sheep populations with lower levels of RSSS sampling. Identification compliance is being evaluated by reviewing reports from slaughter plants on the proportion of animals with appropriate identification. Additional analyses remain, including defining the most appropriate economic analyses, and comparing the surveillance system with developing surveillance standards. The working group hopes to have a draft written report for review by the end of the year.

Giving the Update on Scrapie Diagnostics and Susceptibility was Katherine O’Roarke, Research Microbiologist, USDA-ARS. "What’s New in Scrapie" -- Biopsy sampling of the third eyelid or tonsillar lymphoid tissue is a useful live animal test for scrapie. The biopsy sample is examined for accumulation of the abnormal prion protein using immunohistochemistry. A joint project conducted by the Veterinary Laboratory Agencies and the Moredun Institute in the United Kingdom has developed an alternative technique in which tissue is collected from the narrow band of lymphoid tissue near the rectal-anal junction. The morphology of the lymphoid follicles is similar in the tonsil, retropharyngeal lymph nodes, third eyelid, and rectal-anal mucosal tissue. A report on more than 300 sheep in the United Kingdom (UK), prepared by Drs. Lorenzo Gonzalez and Jeffrey Martin, will describe the sensitivity, specificity, and optimal collection interval for this technique in a variety of breeds of British sheep. ARS has done a preliminary evaluation of the technique in US sheep. Samples of third eyelid and rectal-mucosal tissue were collected from 56 sheep. Forty-two (42) sheep had negative biopsies at both sites; most of these sheep have been necropsied and no PrP-d was found in retropharyngeal lymph node or tonsil, showing good agreement with the antemortem biopsies. Fourteen (14) sheep had positive rectal biopsy samples; of those, only 12 had positive eyelid biopsies. These sheep will be monitored for disease development. However, the protocol is identical for all samples and it is probable that these sheep represent false negative third eyelid results. Abstracts of reports on the UK studies indicate that sensitivity of the test was 70% in the UK; similar large scale testing on US sheep is necessary. The biopsy tissue is somewhat difficult to handle in the tissue processing laboratory and adaptation to an ELISA format may improve test performance.

Alexia McKnight, Assistant Professor of Radiology, University of Pennsylvania, reviewed magnetic resonance imaging (MRI) diagnostics before the committee. A synopsis containing references is attached at the end of this report. Dr. McKnight asked the question, "could MRI be a cost-effective screening test, estimated at $25-30 each with results immediately available." The committee feels that it is not practical as compared to other alternatives currently available. However, the committee expressed interest in future reference to this technology.

Dr. Diane Sutton lead the Uniform Methods and Rules (UM&R) and Regulatory Issues Discussion. Several modifications to the UM&R were discussed. Eight issues were identified and communicated to the APHIS scrapie program coordinator. The committee acknowledged that APHIS and the industry is adequately addressing the year-to-year industry concerns.

Dr. Kris Petrini representing the North Central United States Animal Health Association District presented five recommendations to the Committee. During the discussions regarding these recommendations it was evident that all five issues had been addressed during the year at this Committee meeting.

The Committee approved a recommendation that USDA-APHIS-VS continue to provide indemnity funds for animals that have been designated for testing in Flocks Under Investigation as an alternative to third eyelid testing after consultation with the designated Scrapie Epidemiologist (DSE) and the Regional Area Epidemiologist (RAE).

The 2004 Resolutions along with their responses were reviewed by the Committee.

A Resolution concerning premises registration and identification was approved by the Committee and forwarded to the Committee on Nominations and Resolutions.

Committee on Scrapie

Status Report-Fiscal Year 2005: Cooperative State-Federal Scrapie Eradication Program

Submitted by Diane Sutton, DVM and Gary Ross, DVM

National Center for Animal Health Programs, APHIS, USDA

In Fiscal Year 2005 the Scrapie Eradication Program focused on: (1) utilization of a genetic based approach to flock clean-up plans; (2) cleaning up infected and source flocks; (3) tracing and testing exposed animals and flocks; (4) expansion of regulatory slaughter surveillance (RSSS); (5) conducting considtent state reviews, (6) producer education; (7) upgrading of the Scrapie National Generic Database and (8) publishing the updated Scrapie Eradication Uniform Methods and Rules (UM&R). The current Scrapie Eradication UM&R is posted at

Consistent State Reviews

States must meet the requirements in 9 CFR 79.6 in order to move sheep and goats in interstate commerce with minimal restrictions. Twenty seven states have enacted the required identification rules, the remaining states have submitted a work plan that describes the steps that will be taken to comply and provided a timeline for completing significant milestones. USDA is conducting onsite scrapie program consistent state reviews and has completed reviews in 12 states. States must be in full compliance by the end of their current rule making cycle. States not in full compliance at that time will be removed from the consistent state list. Removal from the list would create a significant impact on the interstate movement of sheep and goats from those States.

Scrapie Flock Certification Program

As of September 30, 2005, there were 1,961 flocks participating in the Scrapie Flock Certification Program (SFCP). Of these flocks 188 were certified flocks, 1,770 were complete monitored flocks, and 3 were selective monitored flocks (figure 2). There were 209 flocks newly enrolled and 53 newly certified (13 with status dates in FY 2005 and 40 with status dates in previous years) in FY 2005 (figure 3).

Infected and Source Flocks

As of September 30, 2005, there were 105 scrapie infected and source flocks. There were a total of 165** new infected and source flocks reported for FY 2005. The total infected and source flocks that have been released in FY 2005 was 128. The ratio of infected and source flocks cleaned up or placed on clean up plans vs. new infected and source flocks discovered in FY 2005 was 1.03 : 1*. In addition 622 scrapie cases were confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2005, of which 130 were RSSS cases. Fifteen cases of scrapie in goats have been reported since 1990. The last goat case was reported in May 2005. Approximately 5,626 animals were indemnified comprised of 49% non-registered sheep, 45% registered sheep, 1.4% non-registered goats and 4.6% registered goats.

Regulatory Scrapie Slaughter Surveillance (RSSS)

RSSS was designed to utilize the findings of the Center for Epidemiology and Animal Health (CEAH) Scrapie: Ovine Slaughter Surveillance (SOSS) study. The results of SOSS can be found at . RSSS started April 1,

2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks for clean-up. During FY 2005 collections increased by 32% overall and by 90% for black and mottled faced sheep improving overall program effectiveness and efficiency as demonstrated by the 26% decrease in percent positive black faced sheep compared to FY 2004. Samples have been collected from 62,864 sheep since April 1, 2003, of which results have been reported for 59,105 of which 209 were confirmed positive. During FY 2005, 33,137 samples were collected from 81 plants. There have been 130 NVSL confirmed positive cases (30 collected in FY 2004 and confirmed in FY 2005 and 100 collected and confirmed in FY 2005) in FY 2005. Face colors of these positives were 114 black, 14 mottled, 1 white and 1 unknown. The percent positive by face color is shown in the chart below.

Scrapie Testing

In FY 2005, 35,845 animals have been tested for scrapie: 30,192 RSSS; 4,742 regulatory field cases; 772 regulatory third eyelid biopsies; 10 third eyelid validations; and 129 necropsy validations (chart 9).

Animal ID

As of October 04, 2005, 103,580 sheep and goat premises have been assigned identification numbers in the Scrapie National Generic Database. Official eartags have been issued to 73,807 of these premises.

*This number based on an adjusted 12 month interval to accommodate the 60 day period for setting up flock plans.

Gerald Wells: Report of the Visit to USA, April-May 1989


The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...


It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...


3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...




To minimise the risk of farmers' claims for compensation from feed

To minimise the potential damage to compound feed markets through adverse publicity.

To maximise freedom of action for feed compounders, notably by
maintaining the availability of meat and bone meal as a raw
material in animal feeds, and ensuring time is available to make any
changes which may be required.




MAFF remains under pressure in Brussels and is not skilled at
handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which
contain illegal traces of ruminant protein. More likely, a few positive
test results will turn up but proof that a particular feed mill knowingly
supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed
compounders are free of it. The longer we can avoid any direct
linkage between feed milling _practices_ and actual BSE cases,
the more likely it is that serious damage can be avoided. ...

SEE full text ;

Date: September 6, 2006 at 7:58 am PST

a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone
on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is
Dairy and poultry feeds were possibly contaminated with ruminant based
477.72 tons
a) Dairy feed, custom, Recall # V-134-6;
b) Custom Dairy Feed with Monensin, Recall # V-135-6.
None. Bulk product
Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on
June 28, 2006.
Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated
recall is complete.
Possible contamination of dairy feeds with ruminant derived meat and bone
1,484 tons
TN and WV

MS, AL, GA, AND TN 11,000+ TONS
Date: August 16, 2006 at 9:19 am PST

Bulk custom made dairy feed, Recall # V-115-6
Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or
about July 14, 2006. FDA initiated recall is ongoing.
Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.
Approximately 2,223 tons

Bulk custom made dairy feed, Recall # V-116-6
Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006.
FDA initiated recall is ongoing.
Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.
1,220 tons

Bulk custom made dairy feed, Recall # V-117-6
Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated
recall is completed.
Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
40 tons
LA and MS

Bulk Dairy Feed, Recall V-118-6
Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA
initiated recall is complete.
Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
7,150 tons

Bulk custom dairy pre-mixes, Recall # V-119-6
Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm
initiated recall is complete.
Possible contamination of dairy animal feeds with ruminant derived meat and
bone meal.
87 tons

Bulk custom dairy pre-mixes, Recall # V-120-6
Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm
initiated recall is complete.
Possible contamination of dairy animal feeds with ruminant derived meat and
bone meal.
350 tons
AL and MS

a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet,
50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet,
50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower,
50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD
Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags,
Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags,
Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher,
50 lb bags, Recall # V-127-6
All products manufactured from 02/01/2005 until 06/20/2006
Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit
on June 20, 2006, and by letter on June 23, 2006.
Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated
recall is ongoing.
Poultry and fish feeds which were possibly contaminated with ruminant based
protein were not labeled as "Do not feed to ruminants".
7,541-50 lb bags
AL, GA, MS, and TN



COMMERCE 27,694,240 lbs
Date: August 6, 2006 at 6:14 pm PST
Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J.
Baker recalled feed products.
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm
initiated recall is complete.
The feed was manufactured from materials that may have been contaminated
with mammalian protein.
27,694,240 lbs



TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
net wt 50 Lbs, Recall # V-110-6;
Recall # V-111-6;
Recall # V-112-6
Product manufactured from 02/01/2005 until 06/06/2006
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and
visit on June 9, 2006. FDA initiated recall is complete.
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
125 tons
AL and FL



Date: August 6, 2006 at 6:19 pm PST
Bulk custom made dairy feed, Recall # V-114-6
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated
recall is ongoing.
Custom made feeds contain ingredient called Pro-Lak, which may contain
ruminant derived meat and bone meal.


Sun Jul 16, 2006 09:22

a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals,
Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg),
Recall # V-080-6;
FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6
a) Bulk
b) None
c) Bulk
d) Bulk
H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and
by press release on June 16, 2006. Firm initiated recall is ongoing.
Possible contamination of animal feeds with ruminent derived meat and bone
10,878.06 tons



Date: June 27, 2006 at 7:42 am PST
Public Health Service
Food and Drug Administration

New Orleans District
297 Plus Park Blvd.
Nashville, TN 37217

Telephone: 615-781-5380
Fax: 615-781-5391

May 17, 2006



Mr. William Shirley, Jr., Owner
Louisiana.DBA Riegel By-Products
2621 State Street
Dallas, Texas 75204

Dear Mr. Shirley:

On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration
(FDA) investigator inspected your rendering plant, located at 509 Fortson
Street, Shreveport, Louisiana. The inspection revealed significant
deviations from the requirements set forth in Title 21, Code of Federal
Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in
Ruminant Feed. This regulation is intended to prevent the establishment and
amplification of Bovine Spongiform Encephalopathy (BSE). You failed to
follow the requirements of this regulation; products being manufactured and
distributed by your facility are misbranded within the meaning of Section
403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act
(the Act).

Our investigation found you failed to provide measures, including sufficient
written procedures, to prevent commingling or cross-contamination and to
maintain sufficient written procedures [21 CFR 589.2000(e)] because:

You failed to use clean-out procedures or other means adequate to prevent
carryover of protein derived from mammalian tissues into animal protein or
feeds which may be used for ruminants. For example, your facility uses the
same equipment to process mammalian and poultry tissues. However, you use
only hot water to clean the cookers between processing tissues from each
species. You do not clean the auger, hammer mill, grinder, and spouts after
processing mammalian tissues.

You failed to maintain written procedures specifying the clean-out
procedures or other means to prevent carryover of protein derived from
mammalian tissues into feeds which may be used for ruminants.

As a result . the poultry meal you manufacture may contain protein derived
from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR
589.2000(e)(1)(i), any products containing or may contain protein derived
from mammalian tissues must be labeled, "Do not feed to cattle or other
ruminants." Since you failed to label a product which may contain protein
derived from mammalian tissues with the required cautionary statement. the
poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the

This letter is not intended as an all-inclusive list of violations at your
facility. As a manufacturer of materials intended for animal feed use, you
are responsible for ensuring your overall operation and the products you
manufacture and distribute are in compliance with the law. You should take
prompt action to correct these violations, and you should establish a system
whereby violations do not recur. Failure to promptly correct these
violations may result in regulatory action, such as seizure and/or
injunction, without further notice.

You should notify this office in writing within 15 working days of receiving
this letter, outlining the specific steps you have taken to bring your firm
into compliance with the law. Your response should include an explanation of
each step taken to correct the violations and prevent their recurrence. If
corrective action cannot be completed within 15 working days, state the
reason for the delay and the date by which the corrections will be
completed. Include copies of any available documentation demonstrating
corrections have been made.

Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S.
Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie,
Louisiana 70001. If you have questions regarding any issue in this letter,
please contact Mr. Rivero at (504) 219-8818, extension 103.



Carol S. Sanchez
Acting District Director
New Orleans District

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused
7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to
non-human primates. We gave two macaques a 5 g oral dose of brain homogenate
from a BSE-infected cow. One macaque developed vCJD-like neurological
disease 60 months after exposure, whereas the other remained free of disease
at 76 months. On the basis of these findings and data from other studies, we
made a preliminary estimate of the food exposure risk for man, which
provides additional assurance that existing public health measures can
prevent transmission of BSE to man.


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a
similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of
disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic
ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula

Published online January 27, 2005

It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.


6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100 grams) was probably given with the benefit of hindsight; particularly if one
considers that later in the same answer Mr Bradley expresses his surprise
that it could take as little of 1 gram of brain to cause BSE by the oral route
within the same species. This information did not become available until the "attack
rate" experiment had been completed in 1995/96. This was a titration experiment
designed to ascertain the infective dose. A range of dosages was used to
ensure that the actual result was within both a lower and an upper limit within the
study and the designing scientists would not have expected all the dose levels to
trigger infection. The dose ranges chosen by the most informed scientists at that
time ranged from 1 gram to three times one hundred grams. It is clear that the
designing scientists must have also shared Mr Bradley's surprise at the results
because all the dose levels right down to 1 gram triggered infection.

Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]

2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. .........

and i think, with time, and testing becomes more and more sensitive, we will all be surprised at just how much is too much, and just how young one might be to spread the agent, even as sub-clinical.

IF i remember correctly, the infamous PURINA FEED MILL incident in Gonzales TEXAS,
where at one feeding, those cows could not have consumed more than......or no more than 5.5 grams...etc. so, how many feedings does a feeder and or dairy calf have in there lifespan ? wouldn't you multiply that by those figures by that ??? be a lot of potential mad cow protein IN COMMERCE, and still is in 2006......tss

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

amplification and transmission, it's not rocket science. ...TSS

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