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
