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graybull

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Just saw that the USDA is trying to track down BSE cow in CA's offspring.

Here is my question......

Is there any evidence that atypical BSE can be passed to offspring?

Thanks for saving me reading all your posts and other research.
 

graybull

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Please disregard......as I believe I have found the answer......

"We actually don’t know if atypical BSE is transmissible at all."

Taken from......

http://www.bseinfo.org/atypicalbse.aspx

So now my question becomes......

Any idea WHY USDA would waste resources and contribute to more public alarm by not only doing this “follow up”……but also issuing press releases to that effect……when based on their own best science…..there is no evidence of transmission of atypical BSE to offspring?
 

flounder

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graybull said:
Just saw that the USDA is trying to track down BSE cow in CA's offspring.

Here is my question......

Is there any evidence that atypical BSE can be passed to offspring?

Thanks for saving me reading all your posts and other research.





say there graybull.


with typical c-type BSE, horizontal transmission of this strain is supposedly very low.


with atypical L-type BASE BSE, that's another question, one that has not been answered yet, but one that should be taken very seriously.


then you have the CWD strains in cervids and scrapie strains. once these strains mutate, become more virulent, such as with the atypical L-type BASE BSE, then there should be much more concern for this type transmission.




please see ;




Vertical Transmission of Bovine Spongiform Encephalopathy Prions Evaluated in a Transgenic Mouse Model

J. Castilla1,
A. Brun1,
F. Díaz-San Segundo1,
F. J. Salguero1,
A. Gutiérrez-Adán2,
B. Pintado2,
M. A. Ramírez2,
L. del Riego1, and
J. M. Torres1,*

+ Author Affiliations



1Centro de Investigación en Sanidad Animal (CISA-INIA), Ctra. de Valdeolmos a El Casar, Valdeolmos, 28130 Madrid, Spain
2Departamento de Reproducción Animal y Conservación de Recursos Zoogenéticos (INIA), Avda. Puerta de Hierro s/n, Madrid 28040, Spain

ABSTRACT

In this work we show evidence of mother-to-offspring transmission in a transgenic mouse line expressing bovine PrP (boTg) experimentally infected by intracerebral administration of bovine spongiform encephalopathy (BSE) prions. PrPres was detected in brains of newborns from infected mothers only when mating was allowed near to the clinical stage of disease, when brain PrPres deposition could be detected by Western blot analysis. Attempts to detect infectivity in milk after intracerebral inoculation in boTg mice were unsuccessful, suggesting the involvement of other tissues as carriers of prion dissemination. The results shown here prove the ability of BSE prions to spread centrifugally from the central nervous system to peripheral tissues and to offspring in a mouse model. Also, these results may complement previous epidemiological data supporting the occurrence of vertical BSE transmission in cattle.



FOOTNOTES
Received 4 November 2004.
Accepted 3 March 2005.
↵*Corresponding author. Mailing address: Centro de Investigación en Sanidad Animal INIA, Valdeolmos, 28130 Madrid, Spain. Phone: 34 91 620 23 00. Fax: 34 91 620 22 47. E-mail: [email protected]
American Society for Microbiology


http://jvi.asm.org/content/79/13/8665.abstract





Envt.18: Mother to Offspring Transmission of Chronic Wasting Disease


Candace K. Mathiason,† Amy Nalls, Kelly Anderson, Jeanette Hayes-Klug, Jenny G. Powers, Nicholas J. Haley and Edward A. Hoover


Colorado State University; Fort Collins, CO USA†Presenting author; Email: [email protected]


We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by four months post infection. Ten fawns were born to these CWD-infected doe— four of the fawns were viable, five were non-viable and one was a first trimester fetus harvested from a CWD-infected doe euthanized at end-stage disease. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn by IHC as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yielded positive results on another fawn at ten days of age. In addition, sPMCA assays have demonstrated amplifiable prions in fetal placental or spleen tissue of three non-viable fawns and mammary tissue of the dams.


Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.



===========================



PPo3-18: A Possible Case of Maternal Transmission of the BSE Agent within Captive Cheetah Affected with Feline Spongiform Encephalopathy

Anna Bencsik, Sabine Debeer, Thierry Petit and Thierry Baron

Afssa; Unité ATNC; Lyon, France; Zoo de la Palmyre; Les Mathes, France

Key words: BSE, FSE, vertical transmission

Introduction. Feline spongiform encephalopathy (FSE) is considered to be related to bovine spongiform encephalopathy (BSE). It has been reported in domestic cats as well as in captive wild cats including cheetahs, first in the United Kingdom (UK) and then in other European countries. In France, several cases were described in cheetahs either imported from UK or born in France. Here we report details of two other FSE cases in captive cheetah. These cases are of particular interest since the 2nd case of FSE in a cheetah born in France, appears most likely due to maternal transmission.1

Results. Complete PrPd study showed the close likeness between the two cheetah cases. The TgOvPrP4 mouse brains infected with cattle BSE and cheetah FSE revealed similar vacuolar lesion profiles, PrPd brain mapping with occurrence of typical florid plaques.

Materials and Methods. Using immunohistochemistry (IHC), pathological form of PrP(PrPd) was analyzed in the brains and peripheral organs of these two cheetahs. Transmission studies to the TgOvPrP4 mouse line were also performed, for comparison with the transmission of cattle BSE. Lesion profiles of the infected transgenic mice were analyzed as well as type and brain distribution of PrPd.

Conclusion. Collectively, these data indicate that both FSE cases harbor the same strain of agent as the cattle BSE agent. Because this is most probably a case of maternal transmission of the disease, this new observation may have some impact on our knowledge of vertical transmission of BSE agent-linked TSEs such as in human variant Creutzfeldt Jakob disease.

References

1. Bencsik et al. PLoS One 2009; 4:6929.



=========================



PPo3-40: Mother to Offspring Transmission of Chronic Wasting Disease

Candace K. Mathiason, Amy V. Nalls, Kelly Anderson, Jeanette Hayes-Klug, Nicholas Haley and Edward A. Hoover

Colorado State University, Department of Microbiology, Immunology and Pathology, Fort Collins, CO USA

Key words: Chronic wasting disease, vertical transmission, muntjac deer

We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by 4 months post infection. Six fawns were born to these CWD-infected doe. Six fawns were born to 6 CWD-infected doe; 4 of the fawns were non-viable. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive results on another fawn at 10 days of age. In addition, sPMCA assays have also demonstrated amplifiable prions in maternal placental (caruncule) and mammary tissue of the dam.

Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.



PRION 2011



landesbioscience.com





International Prion Congress: From agent to diseaseSeptember 8–11, 2010Salzburg, Austria





=============================




Executive Summary








7. The executive summary must not exceed 2 sides in total of A4 and should be understandable to the intelligent non-scientist.

It should cover the main objectives, methods and findings of the research, together with any other significant events and options for new work.









The purpose of this study was to investigate whether sheep, of various PrP genotypes, experimentally infected with BSE could transmit the disease to their offspring. The genotypes of the ewes were chosen as most susceptible (AQ/AQ) through to least susceptible (AR/AR) when challenged orally with BSE. A number of unchallenged ewes were mixed with these sheep to monitor for adventitious lateral transmission of disease.



The sheep were NPU Cheviots which do not always show BSE clinical signs after experimental challenge.Offspring therefore fell into three groups: those from mothers that did develop clinical BSE, those from challenged ewes which remained healthy, and those from control unchallenged ewes.



Over the course of the study the ewes produced eight lamb crops and a total of 144 lambs which were observed for at least 5 years. The lambs were grouped together based on gender while the parturient ewes were mixed together just prior to and after lambing. Ewes were penned separately during the perinatal phase. At weaning the lambs joined the larger groups of lambs.



None of the 144 lambs showed any evidence of contracting BSE from the experimentally dosed sheep, however, two sheep plus one of the unchallenged control ewes did have pathology and PrPSc Western blotting pattern which were indicative of atypical scrapie.



Our results (statistically analysed) suggest that maternal transmission of BSE under the experimental conditions of this study could only occur in NPU Cheviots at a maximum rate less than 28%. However, a further study in sheep (Bellworthy et al 2005) showed that natural transmission of BSE was possible within an experimental flock under certain circumstances although within the 28% margin found in the present study. Studies in goats with BSE (Foster et al 1999) showed a maximum possible transmission rate of 5% while cattle studies (Wilesmith et al 1997) have suggested a rate no higher that 10%.

Taken together these studies provide good evidence that should BSE have infected sheep, it is unlikely to have be maintained within the population by the maternal transmission route.






http://randd.defra.gov.uk/Default.aspx?Menu=Menu&Module=More&Location=None&Completed=0&ProjectID=6168







SEE MORE HERE ON THE POTENTIAL FOR VERTICAL TRANSMISSION WITH TSE PRION DISEASE ;



http://creutzfeldt-jakob-disease.blogspot.com/2009/12/is-there-evidence-of-vertical.html







spontaneous mutation is a myth. never proven for any natural field case of bse. it's one of three hypothesis put forward by scientist, and the spontaneous mutation theory is at the bottom of the list. sporadic and or spontaneous CJD, which is 85%+ of all CJD, simply means from 'unknown source/origin'. it does NOT mean that 85%+ of all CJD i.e. sporadic/sponaneous just happens from a bad funked out twisted the wrong way protein. atypical L-type BSE or BASE, has been linked to sporadic CJD. it's looking more and more like a link from the L-type atypical BSE to the Transmissible Mink Encephalopathy TME. that would mean L-type BASE BSE would have been in North America for decades. the lies about the feed not being a source for atypical mad cow disease is just that, lies. a day or two before the 4th mad cow, I put out an update on Canada BSE and Canada CJD in two links. see at the bottom...terry




America's Mad Cow crisis by John Stauber


Wednesday, April 25, 2012


America's Mad Cow Crisis by John Stauber



http://www.commondreams.org/view/2012/04/26-1



http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/americas-mad-cow-crisis-by-john-stauber.html




Wednesday, April 25, 2012

4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012


http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/4th-mad-cow-disease-usa-california.html



Monday, April 23, 2012

CREUTZFELDT JAKOB DISEASE CJD HUMAN TSE CANADA UPDATE 2012

http://creutzfeldt-jakob-disease.blogspot.com/2012/04/creutzfeldt-jakob-disease-cjd-human-tse.html




Monday, April 23, 2012

BOVINE SPONGIFORM ENCEPHALOPATHY BSE CJD TSE PRION DISEASE UPDATE CANADA 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/bovine-spongiform-encephalopathy-bse.html




Wednesday, April 25, 2012

USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 – 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/usa-mad-cow-disease-and-cjd-there-from.html





kind regards,
terry
 

flounder

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graybull said:
Please disregard......as I believe I have found the answer......

"We actually don’t know if atypical BSE is transmissible at all."

Taken from......

http://www.bseinfo.org/atypicalbse.aspx

So now my question becomes......

Any idea WHY USDA would waste resources and contribute to more public alarm by not only doing this “follow up”……but also issuing press releases to that effect……when based on their own best science…..there is no evidence of transmission of atypical BSE to offspring?




Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate

Emmanuel E. Comoy1*, Cristina Casalone2, Nathalie Lescoutra-Etchegaray1, Gianluigi Zanusso3, Sophie Freire1, Dominique Marcé1, Frédéric Auvré1, Marie-Magdeleine Ruchoux1, Sergio Ferrari3, Salvatore Monaco3, Nicole Salès4, Maria Caramelli2, Philippe Leboulch1,5, Paul Brown1, Corinne I. Lasmézas4, Jean-Philippe Deslys1

1 Institute of Emerging Diseases and Innovative Therapies, CEA, Fontenay-aux-Roses, France, 2 Istituto Zooprofilattico Sperimentale del Piemonte, Turin, Italy, 3 Policlinico G.B. Rossi, Verona, Italy, 4 Scripps Florida, Jupiter, Florida, United States of America, 5 Genetics Division, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America

Abstract Top Background Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne transmission of prions from slaughtered cattle with classical Bovine Spongiform Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic in aging cattle, were recently identified at slaughterhouses throughout Europe and North America, raising a question about human susceptibility to these new prion strains.

Methodology/Principal Findings Brain homogenates from cattle with classical BSE and atypical (BASE) infections were inoculated intracerebrally into cynomolgus monkeys (Macacca fascicularis), a non-human primate model previously demonstrated to be susceptible to the original strain of cBSE. The resulting diseases were compared in terms of clinical signs, histology and biochemistry of the abnormal prion protein (PrPres). The single monkey infected with BASE had a shorter survival, and a different clinical evolution, histopathology, and prion protein (PrPres) pattern than was observed for either classical BSE or vCJD-inoculated animals. Also, the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine.

Conclusion/Significance Our results point to a possibly higher degree of pathogenicity of BASE than classical BSE in primates and also raise a question about a possible link to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning epidemic of classical BSE, the occurrence of atypical strains should temper the urge to relax measures currently in place to protect public health from accidental contamination by BSE-contaminated products.



Citation: Comoy EE, Casalone C, Lescoutra-Etchegaray N, Zanusso G, Freire S, et al. (2008) Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate. PLoS ONE 3(8): e3017. doi:10.1371/journal.pone.0003017

Editor: Neil Mabbott, University of Edinburgh, United Kingdom

Received: April 24, 2008; Accepted: August 1, 2008; Published: August 20, 2008

Copyright: © 2008 Comoy et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This work has been supported by the Network of Excellence NeuroPrion.

Competing interests: CEA owns a patent covering the BSE diagnostic tests commercialized by the company Bio-Rad.

* E-mail: [email protected]





snip...



In summary, we have transmitted one atypical form of BSE (BASE) to a cynomolgus macaque monkey that had a shorter incubation period than monkeys infected with classical BSE, with distinctive clinical, neuropathological, and biochemical features; and have shown that the molecular biological signature resembled that seen in a comparatively uncommon subtype of sporadic CJD. We cannot yet say whether BASE is more pathogenic for primates (including humans) than cBSE, nor can we predict whether its molecular biological features represent a clue to one cause of apparently sporadic human CJD. However, the evidence presented here and by others justifies concern about a potential human health hazard from undetected atypical forms of BSE, and despite the waning epizoonosis of classical BSE, it would be premature to abandon the precautionary measures that have been so successful in reversing the impact of cBSE. We would instead urge a gradual, staged reduction that takes into account the evolving knowledge about atypical ruminant diseases, and both a permanent ban on the use of bovine central nervous system tissue for either animal or human use, and its destruction so as to eliminate any risk of environmental contamination.





http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0003017






Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model




Nadine Mestre-Francés, Simon Nicot, Sylvie Rouland, Anne-Gaëlle Biacabe, Isabelle Quadrio, Armand Perret-Liaudet, Thierry Baron, and Jean-Michel Verdier



We report transmission of atypical L-type bovine spongiform encephalopathy to mouse lemurs after oral or intracerebral inoculation with infected bovine brain tissue. After neurologic symptoms appeared, transmissibility of the disease by both inoculation routes was confi rmed by detection of disease-associated prion protein in samples of brain tissue.



snip...


Conclusions

We demonstrated that the agent of L-BSE can be transmitted by the oral route from cattle to mouse lemurs. As expected, orally inoculated animals survived longer than IC-inoculated animals. Orally inoculated lemurs had less severe clinical signs and symptoms, with no evidence of motor dysfunction. It was previously suggested that the agent of L-BSE might be involved in the foodborne transmission of a prion disease in mink (11,12), a species in which several outbreaks of transmissible mink encephalopathy had been identifi ed, notably in the United States (13).

Our study clearly confi rms, experimentally, the potential risk for interspecies oral transmission of the agent of L-BSE. In our model, this risk appears higher than that for the agent of classical BSE, which could only be transmitted to mouse lemurs after a fi rst passage in macaques (14). We report oral transmission of the L-BSE agent in young and adult primates. Transmission by the IC route has also been reported in young macaques (6,7). A previous study of L-BSE in transgenic mice expressing human PrP suggested an absence of any transmission barrier between cattle and humans for this particular strain of the agent of BSE, in contrast to fi ndings for the agent of classical BSE (9). Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.




http://wwwnc.cdc.gov/eid/article/18/1/pdfs/11-1092.pdf



http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/oral-transmission-of-l-type-bovine.html





Wednesday, March 31, 2010




Atypical BSE in Cattle




To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.




This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.




http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2




Thursday, August 12, 2010




Seven main threats for the future linked to prions




First threat




The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.




***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.




Second threat




snip...




http://www.neuroprion.org/en/np-neuroprion.html










TSS
 

Faster horses

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You just don't get it do you, flounder?
You just DID what graybull DID NOT want you to do.
And in fact, you did it twice.

You are not making any friends here and as far as I know,
you aren't 'educating' anyone, cuz no one reads those long
rambling posts you are famous for.

You are wasting your time.
 
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