Detection of CWD prions in naturally infected white-tailed deer fetuses and gestational tissues by PMCA
2021 Sep 15;11(1):18385. doi: 10.1038/s41598-021-97737-y.
Detection of CWD prions in naturally infected white-tailed deer fetuses and gestational tissues by PMCA
Francisca Bravo-Risi 1, Paulina Soto 1, Thomas Eckland 1, Robert Dittmar 2, Santiago Ramírez 1, Celso S G Catumbela 1, Claudio Soto 1, Mitch Lockwood 2, Tracy Nichols 3, Rodrigo Morales 4 5
PMID: 34526562 PMCID: PMC8443553 DOI: 10.1038/s41598-021-97737-y
Abstract
Chronic wasting disease (CWD) is a prevalent prion disease affecting cervids. CWD is thought to be transmitted through direct animal contact or by indirect exposure to contaminated environmental fomites. Other mechanisms of propagation such as vertical and maternal transmissions have also been suggested using naturally and experimentally infected animals. Here, we describe the detection of CWD prions in naturally-infected, farmed white-tailed deer (WTD) fetal tissues using the Protein Misfolding Cyclic Amplification (PMCA) technique. Prion seeding activity was identified in a variety of gestational and fetal tissues. Future studies should demonstrate if prions present in fetuses are at sufficient quantities to cause CWD after birth. This data confirms previous findings in other animal species and furthers vertical transmission as a relevant mechanism of CWD dissemination.
>>>Here, we describe the detection of CWD prions in naturally-infected, farmed white-tailed deer (WTD) fetal tissues using the Protein Misfolding Cyclic Amplification (PMCA) technique. <<<
This is the first report of prion infectivity within the cervid pregnancy microenvironment, revealing a source of fetal CWD exposure prior to the birthing process, maternal grooming, or encounter with contaminated environments.
Experimental details were presented illustrating how easily CWD spreads from animal to animal including by contact with ordinary body secretions, environmental contamination and with evidence of maternal transmission (from mother to unborn offspring).
PRION 2018 CONFERENCE
WA1 An overview— Chronic Wasting Disease mother to offspring transmission studies conducted at Colorado State University
Nalls AV1‡, McNulty EE1‡, Hoover C1, Hoover EA1, Wild M2, Powers J2, Selariu A1, Mathiason CK1 1Colorado State University, Fort Collins, CO USA, 2 National Park Services, Fort Collins, CO USA.
Chronic wasting disease (CWD) demonstrates remarkable transmission efficiency among captive and free-ranging cervid populations. Intrigued by this facile transmission, we designed a series of studies to determine the potential for CWD transmission from mother to offspring. Viable offspring born to early or late-stage CWD-infected Reeves‘ muntjac dams demonstrated lymphoid biopsy positivity as early as 40 days post birth and developed clinical disease in 2-5 years. Prion infectivity was validated in the milk and colostrum collected from these dams via oral infection studies in naïve fawns, providing a potential mechanism for maternal transmission. High nonviability (~60%) was noted in full-term offspring born to this cohort of CWD-infected muntjac dams. Tissues harvested from the nonviable offspring contained prion seeding activity, suggesting that CWD had been trafficked from mother-to- offspring during gestation. Gestational timing of CWD transfer was assessed by analysis of in utero harvested tissues from a second cohort of preclinical and clinical CWD-infected muntjac dams, and it was found that transmission can occur as early as the first trimester of pregnancy. The next series of studies were initiated to determine if this was a phenomenon of experimental infection, or whether it also occurs in naturally-infected cervids. In collaboration with the National Park Service we evaluated in utero derived tissues from healthy free-ranging elk dams whose habitat is a known CWD endemic region.
Prion seeding activity was detected in fetal tissues harvested from several preclinical CWD positive naturally-infected dams in this population. To begin to unravel the biological relevance of these findings we initiated mouse bioassay to assess the infectivity of the pregnancy microenvironment of muntjac dams. Uterus, placenta, ovary and amniotic fluid contained prion infectivity. Ongoing mouse bioassay will further define infectivity in fetal and reproductive tissues harvested from free-ranging naturally-exposed elk dams.
This work has led to a better understanding of the transmission dynamics of CWD, demonstrating that:
(i) fetuses of preclinical infected cervid dams are exposed to CWD long before exposure to maternal saliva or contaminated environments,
(ii) CWD mother-to- offspring transmission occurs in free-ranging naturally-exposed cervid populations, and
(iii) the Reeves‘ muntjac deer can be used to further explore mechanisms of in utero prion trafficking and the potential for multigenerational CWD transmission.
PRION 2018 CONFERENCE
P74 High Prevalence of CWD prions in male reproductive samples
Carlos Kramm (1,2), Ruben Gomez-Gutierrez (1,3), Tracy Nichols (4), Claudio Soto (1) and Rodrigo Morales (1) (1) Mitchell Center for Alzheimer´s disease and Related Brain Disorders, Dept. of Neurology, University of Texas Houston Medical School, Houston, TX 77030, USA (2) Universidad de los Andes, Facultad de Medicina, Av. San Carlos de Apoquindo 2200, Las Condes, Santiago, Chile (3) Universidad de Málaga, Málaga, Spain (4) National Wildlife Research Center, United States Department of Agriculture, Fort Collins, CO 80521, USA.
Chronic wasting disease (CWD) is a highly infectious and fatal illness affecting captive and freeranging cervids. Mother-to-offspring prion transmission has been described in some animal prion diseases, including CWD. However, few studies have been performed to analyze the prevalence of CWD prions in reproductive male tissues and fluids. Here, we optimized the Protein Misfolding Cyclic Amplification (PMCA) assay for the efficient detection of CWD prions in these samples. This study was done in collaboration with United States Department of Agriculture (USDA) scientists who provided blindly field-collected testes, epididymis and seminal fluid samples from 21 white-tailed deer that were analyzed for prion infection by post-mortem histological studies in brain stem and lymphoid tissues. The results showed positive CWD prion detection in testes, epididymis and seminal fluid samples. A high prevalence of CWD-PrPSc was found in samples collected at the late-presymptomatic stage of the disease. Our results showed a correlation between the presence of CWD-PrPSc in male reproductive organs and blood.
These findings demonstrate a high efficiency of CWD prion detection by PMCA in testes, epididymis and seminal fluid, and offer a possibility for a routine screening of semen samples to be commercially distributed for artificial insemination. Our results may uncover new opportunities to understand the mechanisms of CWD spreading and decrease putative interindividual transmission associated to insemination using CWD contaminated specimens. END...TSS
Superovulation and embryo recovery in Red deer (Cervus elaphus ) hinds.
Fennessy PF1, Fisher MW, Shackell GH, Mackintosh CG. Author information 1Invermay Agricultural Centre Private Bag Mosgiel New Zealand.
Abstract
In two experiments, Red deer hinds were synchronized with intravaginal progesterone and were given 4 d of treatment (3 d before progesterone withdrawal and 1 d after) with an ovine follicle stimulating hormone (FSH) preparation which had a claimed low level of luteinizing hormone (LH) contamination. In Experiment 1, 12 hinds received one of four FSH levels by osmotic minipump. Hinds were run with fertile stags, and laparotomy and embryo recovery were performed 9 d after progesterone withdrawal. The ovulation rates (mean of three hinds per dosage) were 1.0, 2.0, 4.3 and 15.3 (number of corpora lutea counted) for estimated daily dosages rates of 0.036, 0.071, 0.11 and 0.14 units FSH preparation/day; the response to the increasing dosage was exponential (P<0 .01="" 0.14="" 11.0="" 18="" 1="" 2="" 3.0="" 34="" 38="" 47="" 63="" 72="" a="" all="" an="" and="" be="" being="" better="" both="" breeding="" by="" considered="" day="" deer="" difference="" div="" eight="" either="" estrus="" experiment="" fertilized="" flushing="" for="" fsh="" function="" higher="" hinds="" improved="" in="" injection.="" intramuscular="" later="" mean="" minipump="" of="" on="" only="" or="" ova="" overall="" ovulation="" p="" performed="" perhaps="" preparation="" previously="" profile="" progesterone="" quality.="" rate="" rates="" received="" recorded="" recovered="" recovery="" red="" respectively="" results="" season="" significant="" significantly="" synchronization.="" than="" that="" the="" those="" to="" transferable="" units="" used="" was="" were="" with=""> http://www.sciencedirect.com/science/article/pii/0093691X89904767 >> ovine follicle stimulating hormone (FSH) F8174 Sigma Follicle Stimulating Hormone from sheep pituitary Synonym: FSH
Louping-ill vaccine sheep scrapie blunder Vaccine for issue had to be free from detectable, living virus and capable of protecting sheep against a test dose of virus applied subcutaneously. The 1935 vaccine conformed to these standards and was issued for inoculation in March as three separate batches labelled 1, 2, and 3. The tissues of 140 sheep were employed to make batch 1 of which 22,270 doses were used; 114 to make batch 2 of which 18,000 doses were used and 44 to make batch 3 of which 4,360 doses were used. All the sheep tissues incorporated in the vaccine were obtained from yearling sheep. During 1935 and 1936 the vaccine proved highly efficient in the prevention of loup-ill and no user observed an ill-effect in the inoculated animals. In September, 1937, two and a half years after vaccinating the sheep, two owners complained that scrapie, a disease which had not before been observed in the Blackface breed, was appearing in their stock of Blackface sheep and further that it was confined to animals vaccinated with louping-ill vaccine in 1935. At that stage it was difficult to conceive that the occurrence could be associated with the injection of the vaccine but in view of the implications, I visited most of the farms on which sheep had been vaccinated in 1935. It was at this point that the investigation reached its dramatic phase; I shall not forget the profound effect on my emotions when I visited these farms and was warmly welcomed because of the great benefits resulting from the application of louping-ill vaccine, wheras the chief purpose of my visit was to determine if scrapie was appearing in the inoculated sheep. The enquiry made the position clear. Scrapie was developing in the sheep vaccinated in 1935 and it was only in a few instances that the owner was associating the occurrence with louping-ill vaccination. The disease was affecting all breeds and it was confined to the animals vaccinated with batch 2. This was clearly demonstrated on a number of farms on which batch 1 had been used to inoculate the hoggs in 1935 and batch 2 to inoculate the ewes. None of the hoggs, which at this time were three- year-old ewes. At this time it was difficult to forecast whether all of the 18,000 sheep which had received batch 2 vaccine would develop scrapie. It was fortunate, however, that the majority of the sheep vaccinated with batch 2 were ewes and therfore all that were four years old and upwards at the time of vaccination had already been disposed of and there only remained the ewes which had been two to three years old at the time of vaccination, consequently no accurate assessment of the incidence of scrapie could be made. On a few farms, however, where vaccination was confined to hoggs, the incidence ranged from 1 percent, to 35 percent, with an average of about 5 percent. Since batch 2 vaccine had been incriminated as a probable source of scrapie infection, an attempt was made to trace the origin of the 112 sheep whose tissues had been included in the vaccine. It was found that they had been supplied by three owners and that all were of the Blackface or Greyface breed with the exception of eight which were Cheviot lambs born in 1935 from ewes which had been in contact with scrapie infection. Some of these contact ewes developed scrapie in 1936-37 and three surviving fellow lambs to the eight included in the batch 2 vaccine of 1935 developed scrapie, one in September, 1936, one in February, 1937, and one in November, 1937. There was, therefore, strong presumptive evidence that the eight Cheviot lambs included in the vaccine althought apparently healthy were, in fact, in the incubative stage of a scrapie infection and that in their tissues there was an infective agent which had contaminated the batch 2 vaccine, rendering it liable to set up scrapie. If that assumption was correct then the evidence indicated that:- (1) the infective agent of scrapie was present in the brain, spinal cord and or spleen of infected sheep: (2) it could withstand a concentration of formalin of 0-35 percent, which inactivated the virus of louping-ill: (3) it could be transmitted by subcutaneous inoculation; (4) it had an incubative period of two years and longer.
Terry S. Singeltary Sr.
>>> Here, in an experimental model of CWD, we have demonstrated the transmission of infectious prions from clinical and subclinical mothers to full-term viable, nonviable and in utero harvested offspring, revealing that the transmission of TSEs from mother to offspring can occur and may be underestimated for all prion diseases. <<<
Sunday, August 25, 2013
Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
IMPORTANCE The facile dissemination of chronic wasting disease within captive and free-range cervid populations has led to questions regarding the transmission dynamics of this disease. Direct contact with infected animals and indirect contact with infectious prions in bodily fluids and contaminated environments are suspected to explain the majority of this transmission. A third mode of transmission, from mother to offspring, may be underappreciated. The presence of pregnancyrelated prion infectivity within the uterus, amniotic fluid, and the placental structure reveals that the developing fetus is exposed to a source of prions long before exposure to the infectious agent during and after the birthing process or via contact with contaminated environments. These findings have impact on our current concept of CWD disease transmission.
THURSDAY, JANUARY 30, 2014
Evidence in Sheep for Pre-Natal Transmission of Scrapie to Lambs from Infected Mothers Evidence in Sheep for Pre-Natal Transmission of Scrapie to Lambs from Infected Mothers
James D. Foster, Wilfred Goldmann, Nora Hunter*
The Roslin Institute and Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian, Scotland, United Kingdom
Abstract
Natural scrapie transmission from infected ewes to their lambs is thought to occur by the oral route around the time of birth. However the hypothesis that scrapie transmission can also occur before birth (in utero) is not currently favoured by most researchers. As scrapie is an opportunistic infection with multiple infection routes likely to be functional in sheep, definitive evidence for or against transmission from ewe to her developing fetus has been difficult to achieve. In addition the very early literature on maternal transmission of scrapie in sheep was compromised by lack of knowledge of the role of the PRNP (prion protein) gene in control of susceptibility to scrapie. In this study we experimentally infected pregnant ewes of known PRNP genotype with a distinctive scrapie strain (SSBP/1) and looked for evidence of transmission of SSBP/1 to the offspring. The sheep were from the NPU Cheviot flock, which has endemic natural scrapie from which SSBP/1 can be differentiated on the basis of histology, genetics of disease incidence and strain typing bioassay in mice. We used embryo transfer techniques to allow sheep fetuses of scrapie-susceptible PRNP genotypes to develop in a range of scrapie-resistant and susceptible recipient mothers and challenged the recipients with SSBP/1. Scrapie clinical disease, caused by both natural scrapie and SSBP/1, occurred in the progeny but evidence (including mouse strain typing) of SSBP/1 infection was found only in lambs born to fully susceptible recipient mothers. Progeny were not protected from transmission of natural scrapie or SSBP/1 by washing of embryos to International Embryo Transfer Society standards or by caesarean derivation and complete separation from their birth mothers. Our results strongly suggest that pre-natal (in utero) transmission of scrapie may have occurred in these sheep.
SNIP...
In conclusion therefore, our study has presented evidence that suggests that transmission of scrapie can occur from the infected mother sheep to her lamb before birth, although it is almost certain not to be the only route by which a lamb can become infected. Further studies are clearly necessary in order to understand the underlying mechanisms and to be able to assess whether the very different placental structures in humans will protect babies from infection if born to CJD infected mothers. Other studies are near completion in our laboratory aimed at clarifying the rate of maternal transmission using scrapie-free sheep of New Zealand origin and therefore without the potential interference from natural scrapie. The ultimate aim of control and eradiation of scrapie infection in sheep clearly depends on understanding all the potential routes of transmission as the use of genetically resistant sheep is not always possible, especially for some rare breeds.
Citation: Foster JD, Goldmann W, Hunter N (2013) Evidence in Sheep for Pre-Natal Transmission of Scrapie to Lambs from Infected Mothers. PLoS ONE 8(11): e79433. doi:10.1371/journal.pone.0079433
Editor: Ilia V. Baskakov, University of Maryland School of Medicine, United States of America
Received September 11, 2013; Accepted September 19, 2013; Published November 18, 2013
Copyright: 2013 Foster 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: The project was funded by Defra (UK Department for the Environment, Food and Rural Affairs) Grant number SE1823 (www.gov.co.uk/defra) with core support funding to the Institute for Animal Health from BBSRC (UK Biotechnology and Biological Sciences Research Council). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.
>>>Further studies are clearly necessary in order to understand the underlying mechanisms and to be able to assess whether the very different placental structures in humans will protect babies from infection if born to CJD infected mothers.<<<
Evidence of in utero transmission of classical scrapie in sheep
John Spiropoulos⇑, Stephen A.C. Hawkins, Marion M. Simmons and Susan J. Bellworthy
+ Author Affiliations Animal Health and Veterinary Laboratories Agency (AHVLA) Weybridge, Addlestone, Surrey KT15 3NB, UK
ABSTRACT
Classical scrapie is one of the Transmissible Spongiform Encephalopathies (TSE), a group of fatal infectious diseases that affect the central nervous system (CNS). Classical scrapie can transmit laterally from ewe to lamb perinatally, or between adult animals. Here we report detection of infectivity in tissues of an unborn foetus, providing evidence that in utero transmission of classical scrapie is also possible.
FOOTNOTES Corresponding Author: John Spiropoulos: Department of Pathology, Animal Health and Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, Email: john.spiropoulos@ahvla.gsi.gov.uk, Tel: +44 (0) 1932 357795, Fax: +44 (0) 1932 357805 Copyright © 2014, American Society for Microbiology. All Rights Reserved.
Tuesday, September 17, 2013
Mother to Offspring Transmission of Transmissible Spongiform Encephalopathy TSE prion disease snip... Maternal CWD infection also appears to result in lower percentage of live birth offspring. In addition, evolving evidence from protein misfolding cyclic amplification (PMCA) assays on fetal tissues suggest that covert prion infection occurs in utero. Overall, our findings demonstrate that transmission of prions from mother to offspring can occur, and may be underestimated for all prion diseases.
snip...
Here, in an experimental model of CWD, we have demonstrated the transmission of infectious prions from clinical and subclinical mothers to full-term viable, nonviable and in utero harvested offspring, revealing that the transmission of TSEs from mother to offspring can occur and may be underestimated for all prion diseases. snip... please see full text ; Tuesday, September 17, 2013
*** Mother to Offspring Transmission of Transmissible Spongiform Encephalopathy TSE prion disease ***
Friday, May 10, 2013
Evidence of effective scrapie transmission via colostrum and milk in sheep
Tuesday, April 30, 2013
Transmission of classical scrapie via goat milk
Veterinary Record2013;172:455 doi:10.1136/vr.f2613
2013
Tuesday, September 17, 2013
*** Mother to Offspring Transmission of Transmissible Spongiform Encephalopathy TSE prion disease *** To date, 125 children have been born to women who later developed CJD [11]. This is concerning because PrPCJD has been detected in the fetal and pregnancy related tissues of a woman infected with CJD [12]. Although decades may pass before the onset of clinical effects associated with such transmission due to a long subclinical carrier state, the probability that these individuals harbor infectious prions remains high.
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: ckm@lamar.colostate.edu
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.
===========================
PPo3tss-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.
=========================
PPo3tss-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
International Prion Congress: From agent to diseaseSeptember 8–11, 2010Salzburg, Austria
Friday, December 23, 2011
Detection of PrPres in Genetically Susceptible Fetuses from Sheep with Natural Scrapie
Monday, November 22, 2010
SHEEP WITH MASTITIS TRANSMIT INFECTIOUS PRIONS THROUGH THE MILK
Saturday, April 12, 2008
Evidence of scrapie transmission via milk
[6] Date: Fri 4 Feb 2005
From: Terry S. Singeltary Sr. flounder@wt.net
Source: Spongiform Encephalopathy Advisory Committee (SEAC), Position Paper, January 2005 [edited]
Thursday, April 26, 2012
Maternal Transmission of the BSE and Birth Cohorts
Friday, December 23, 2011
Detection of PrPres in Genetically Susceptible Fetuses from Sheep with Natural Scrapie
Monday, November 22, 2010
SHEEP WITH MASTITIS TRANSMIT INFECTIOUS PRIONS THROUGH THE MILK
Saturday, April 12, 2008
Evidence of scrapie transmission via milk
[6] Date: Fri 4 Feb 2005
From: Terry S. Singeltary Sr. flounder@wt.net
Source: Spongiform Encephalopathy Advisory Committee (SEAC), Position Paper, January 2005 [edited]
Position Statement: Maternal Transmission of variant Creutzfeldt-Jakob disease
Issue: 1. The Chief Medical Officer for England asked SEAC to consider current evidence and comment on the potential transmission of variant Creutzfeldt-Jakob disease (vCJD) from mother to child via human breast milk. In utero transmission was also considered. The committee also commented on the scientific basis of a risk reduction measure for possible transmission of vCJD via banked breast milk.
Background: 2. No diagnostic test is currently available for the detection of abnormal PrP in milk. Research is under way to develop tests to screen for the possible presence of abnormal prion protein (PrP) in milk samples from cattle experimentally infected with BSE [A joint FSA/SEAC milk working group is monitoring and providing advice on this research carried out at the Veterinary Laboratories Agency.] These modified tests may also be applicable to human milk. However, it is not yet clear when/if a reliable test will be available.
3. A small number of breast milk banks in the UK supply highly vulnerable premature babies for whom no milk may be available from the mother. A model developed by the Department of Health to assess the effect of pooling breast milk from multiple donors on the possible risks of transmission of vCJD via breast milk banks was considered.
4. There is some, albeit limited, published epidemiological and experimental research on maternal transmission of prion diseases. There are also unpublished surveillance data of children born to vCJD cases from the National CJD Surveillance Unit and UK surveillance of neurological illness in children which might inform on potential risks of maternal transmission. Breast milk banks:
5. There is no evidence that vCJD infectivity has ever been transmitted through breast milk. However, a theoretical risk exists. Modelling studies clearly show that the practice of pooling breast milk increases the number of donors to which a recipient is exposed and thereby increases the potential risk of an infant receiving milk contaminated with vCJD infectivity. The theoretical risk of infection can be minimised by not pooling the milk, by the use of individual hand operated breast milk pumps for single donors, and by the use of single-use sterilised bottles for collection. In addition, available evidence suggests that infection/inflammation of the breast results in increased lymphocytes in milk and therefore increased risk of infectivity. This risk would be minimised if milk from donors showing signs of infection were not used.
6. The committee suggested that, if practicable, milk could be stored for an appropriate period of time to allow the health status of donors to be monitored, before it is released. However, information was not available to the committee on whether long-term storage of human milk is detrimental to its nutritional quality. Maternal transmission
7. There is evidence from animal studies for low-level maternal transmission of prions in cattle and sheep. This transmission may occur in utero, via milk and/or perinatally. However, the possibility that this putative maternal transmission might have been due to another mode of transmission, for example through a contaminated environment or feed, cannot be ruled out.
8. In contrast, in humans there is no evidence for maternal transmission in cases of familial prion disease, other than the transfer of a mutant form of the PrP gene, and there is no evidence of maternal transmission of Kuru [a chronic, progressive, uniformly fatal nervous system disorder caused by prions, associated with cannibalism among the Fore tribe and neighboring peoples in New Guinea. - CopyEd.PG]. However, compared with other human prion diseases vCJD may pose a greater risk because of the greater involvement of the lymphoreticular system in vCJD pathogenesis. Although, breast tissue (and placenta) from a single vCJD case tested negative for PrPvCJD, transfer of infectivity to breast milk may depend on the physiological status of the mammary gland. Similar tests or infectivity bioassays have not been conducted on breast tissue from lactating patients with vCJD.
9. A published study suggesting transmission of sCJD in colostrum (ref. 1) was considered unreliable because tissues not normally associated with high levels of infectivity (blood and placenta) showed equivalent infectivity to that of the brain in this study.
10. Analysis of prospective surveillance data of UK children born to mothers with, or that had subsequently developed clinical vCJD, provide no evidence for maternal transmission of vCJD. However, the number of cases is very small and the incubation period of vCJD, if transmitted from mother to child, is unknown and so the children may yet be too young to have developed symptoms.
11. The phenotype of BSE infection in humans expressing PrP genotypes other than M/M at codon 129 is not known. Given recently published studies in mice expressing the human PrP gene (ref. 2), which suggest that the human PrP genotype may affect disease phenotype, the committee considered it very important that undiagnosed neurological diseases be carefully monitored. In this respect, amongst others, it is recommended that the careful monitoring of neurological illnesses through the PIND surveillance of children (ref. 3) continue. Conclusions
12. In summary, there is currently no epidemiological evidence for maternal transmission of vCJD, including transmission via breast milk. However, there is a hypothetical risk. Although available evidence is limited and mostly indirect rather than direct, this risk, if any, appears to be low. As a risk cannot be excluded, a watching brief should be maintained.
References: (1) Tamai Y et al. Demonstration of the transmissible agent in tissue from a pregnant woman with CJD. New Eng J Med 1992 327, 649. (2) Wadsworth et al. Human prion protein with valine 129 prevents expression of variant CJD phenotype. Science. 2004 306, 1793-1796. (3) Devereux G et al. Variations in neurodegenerative disease across the UK: findings from the national study of Progressive Intellectual and Neurological Deterioration (PIND). Arch DisChild. 2004 89, 8-12. -- Terry S. Singeltary Sr. flounder@wt.net
****** P.4.31 Prion infectivity in milk from ARQ/ARQ sheep experimentally infected with Scrapie and MAEDI-VISNA virus
Ciriaco Ligios1, Maria Giovanna Cancedda1, Antonello Carta2, Cinzia Santucciu1 Caterina Maestrale1, Francesca Demontis1, Sonia Attene1, Maria Giovanna Tilocca1, Cristiana Patta1, Massimo Basagni5, Paola Melis1, James C. De- Martini3, Christina Sigurdson4 1Istituto Zooprofilattico Sperimentale della Sardegna, Italy; 2Research Unit: Genetics and Biotechnology, DIRPA, AGRIS Sardinia, Italy; 3Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA; 4Department of Pathology, School of Medicine, University of California San Diego, USA; 5Prion Diagnostica Rho, Italy
Background: Scrapie in sheep is characterized by the deposition of misfolded and aggregated prion protein (PrPSc) in the central nervous system (CNS) and within the lymphoreticular system (LRS). PrPSc was shown to accumulate in organs beyond the CNS and the LRS when lymphofollicular or granulomatous inflammation was also present.
Objectives: Our aim was to determine whether ectopic PrPSc accumulation in the inflamed mammary gland of sheep with scrapie results in infectious prion secretion into the milk. Methods: We fed approximately 1.1 - 2.1 L of milk from sheep with lymphofollicular mastitis and clinical scrapie to each of 8 ARQ/ARQ lambs derived from scrapie-free flocks. The milk donor sheep had been previously inoculated with Maedi-Visna virus (MVV) intratracheally and intravenously and scrapie brain homogenate orally. In addition, 3 ARQ/ARQ lambs were fed approximately 1.4 – 1.7 L of milk from ARQ/ARQ sheep that had been experimentally infected with only scrapie. Additional control ARQ/ARQ lambs were inoculated with scrapie brain homogenate only, or with milk from uninfected sheep.
Results: Two lambs which had received milk from sheep with mastitis and scrapie developed clinical signs of scrapie at 677 and 745 days post-inoculation. One additional clinically healthy lamb from this group, which was sacrificed for a cause unrelated to scrapie, was found to have PrPSc in brain and tonsil. The control lambs and those which received milk from sheep affected only with scrapie are, to date, clinically healthy.
Discussion: This is the first evidence of clinical scrapie in sheep fed milk from scrapie sick sheep. The experiment is ongoing, however these preliminary results indicate that milk and/or colostrum from ARQ/ARQ sheep with clinical scrapie and lymphofollicular mastitis could contribute to scrapie transmission.
Monday, August 03, 2009
Prions Are Secreted in Milk from Clinically Normal Scrapie-Exposed Sheep
Journal of Virology, August 2009, p. 8293-8296, Vol. 83, No. 16 0022-538X/09/$08.00+0 doi:10.1128/JVI.00051-09 Copyright © 2009, American Society for Microbiology. All Rights Reserved.
TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY
a non-profit Swiss Foundation
(January, 2009) TAFS1 STATEMENT ON TRANSMISSION OF SCRAPIE VIA MILK
Prions in Milk from Ewes Incubating Natural Scrapie
ProMED-mail Archive Number 20050211.0467
Published Date 11-FEB-2005 Subject PRO/AH/EDR> CJD (new var.) update 2005 (02)
snip...
****** [3] Date: Thu 20 Jan 2005
From: Terry S. Singeltary Sr. Chronic Lymphocytic Inflammation Specifies the Organ Tropism of Prions Chronic Lymphocytic Inflammation Specifies the Organ Tropism of Prions
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[The following is the summary of a paper by Mathias Heikenwalder and 8 others, published in Science online, 10.1126/science.1106460, Thu 20 Jan 2005 . This paper describes work that illustrates that chronic inflammatory conditions may affect and expand the natural and iatrogenic transmission of prions - Mod.CP]
Prions typically accumulate in nervous and lymphoid tissues. Because proinflammatory cytokines and immune cells are required for lymphoid prion replication, we tested whether inflammatory conditions affect prion pathogenesis. We administered prions to mice with 5 inflammatory diseases of kidney, pancreas or liver. In all cases, chronic lymphocytic inflammation enabled prion accumulation in otherwise prion-free organs. Inflammatory foci consistently correlated with lymphotoxin upregulation and ectopic induction of PrPC-expressing FDC-M1+ cells, whereas inflamed organs of mice lacking lymphotoxin-alpha or its receptor accumulate neither PrPSc nor infectivity upon prion inoculation. By expanding the tissue distribution of prions, chronic inflammatory conditions may act as modifiers of natural and iatrogenic prion transmission.
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[4] Date: Thu 20 Jan 2005 From: Terry S. Singeltary Sr. Source: Reuters News Agency, Thu 20 Jan 2005 [edited] Study Finds that Illness May Promote Spread of Mad Cow Prion
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****** [4] Date: Thu 20 Jan 2005 From: Terry S. Singeltary Sr. Source: Reuters News Agency, Thu 20 Jan 2005 [edited]
Study Finds that Illness May Promote Spread of Mad Cow Prion
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The agent that transmits mad cow disease and related diseases may spread further in the body of an animal suffering from certain illnesses, scientists said on Thu 20 Jan 2005. Their finding raises the question of whether measures aimed at curbing the spread of mad cow disease, or bovine spongiform encephalopathy (BSE), are adequate, the researchers said.
Tests on mice showed that prions, the protein-like fragments that transmit BSE and related diseases [e.g. variant Creutzfeldt-Jakob disease in humans], can show up in organs they are not supposed to if the mouse has an inflammatory condition. Scientists have believed that BSE-causing prions are limited to the brain, spleen, spinal cord and lymph tissue, although some tests have suggested blood and muscle tissue may also harbor the prions. The latest study, published in the journal Science, suggests prions may also sometimes be found in the kidney, pancreas and liver. "We administered prions to mice with 5 inflammatory diseases of kidney, pancreas or liver," wrote the researchers, led by top prion expert Dr. Adriano Aguzzi of the University Hospital of Zurich in Switzerland.
Aguzzi and colleagues in Britain and the United States inoculated specially bred mice with prions and checked to see if the prions spread in their bodies when the mice had an inflammatory condition. This is because other studies had suggested that prions might be attracted to immune system inflammatory cells. "In all cases, chronic lymphocytic inflammation enabled prion accumulation in otherwise prion-free organs," the researchers wrote.
BSE peaked in British cattle herds in the mid-1990s, and a few cases have been reported in other countries. Canada reported its 3rd case this month. People who eat BSE-infected beef products can develop a related human brain disease called variant Creutzfeldt-Jakob disease or vCJD. There is no treatment or cure. [As of 4 Feb 2005, so far in the UK for the year 2005 there have 8 referrals of suspected CJD; and there have been 8 deaths from sporadic CJC, one from GSS and none from familial, iatrogenic or variant CJD. - Mod.CP]. It has killed 148 Britons, and 5 [now 6] Britons are alive with the disease, according to the British Department of Health's monthly report on the disease. The World Health Organization says it has reports of 6 cases in France, one in Ireland, one in Italy, one in Canada and one in the United States [and one in Japan: see; ProMED-mail post "CJD (new var.) - Japan: death 20050204.0381" - Mod.CP]
Experts believed BSE first appeared when cattle were fed improperly rendered remains of sheep infected with scrapie, a related disease. In 1997, the United States and Canada imposed animal feed bans, and have mandated the removal of materials believed to carry infectious prions. These include the skull, brain, nerves attached to the brain, eyes, tonsils, spinal cord and attached nerves, plus a portion of the small intestine. The study suggests that even symptom-free animals may also have prions in their liver, kidney, and pancreas.
-- Terry S. Singeltary Sr.
****** [5] Date: Fri 21 Jan 2005 From: ProMED-mail Souce: New York Times, Fri 21 Jan 2005 [edited]
Study Finds Broader Reach for Mad Cow Proteins
----------------------------------------------
Mad cow disease has long been thought to occur in just the brains and nervous systems of infected animals. But scientists are reporting today that the proteins thought to cause the disease can travel to other organs as well. The research is based on experiments with mice, but if it is borne out in other species, it may suggest that no part of an infected animal is safe to eat. The disease leads to a fatal brain disease in humans [variant Creutzfeldt-Jakob disease].
In the mouse experiments, reported in the journal Science [see [3] above], researchers in Switzerland found that prions, proteins that are the infectious agent in mad cow disease, follow immune cells, called lymphocytes, in the body. When mice were given chronic infectious diseases of the liver, kidney and pancreas and then inoculated with prions, the prions made their way to the infected organs. Dr. Adriano Aguzzi, a neuropathologist at the University Hospital in Zurich, who led the experiments, said this meant that cows and sheep infected with prions could harbor the disease in any inflamed organ.
But Dr. David R. Smith, a veterinarian at the University of Nebraska, said the research did not raise alarms about American beef. For one thing, he said, livestock with obvious signs of systemic infection, like a fever, are not allowed into the food supply. And most American cattle are slaughtered while they are young and at reduced risk of infection.
Many countries, including the United States, require the removal of skulls, brains, eyes, spinal cords and other nervous tissues from slaughtered animals because prions are known to accumulate in those tissues. Even in countries with mad cow disease, mainly in Europe, meat is considered safe if those tissues are removed, Dr. Aguzzi said. But the disease could spread more readily if infections are not obvious or if inspections are sloppily done, he said.
[Byline: Sandra Blakeslee]
-- ProMED-mail
****** [6] Date: Fri 4 Feb 2005 From: Terry S. Singeltary Sr.
****** snip...
ProMED-mail promed@promedmail.org
******[6]Date: Fri 4 Feb 2005
From: Terry S. Singeltary Sr.
Source: Spongiform Encephalopathy Advisory Committee (SEAC), Position Paper, January 2005 [edited]
snip...
******[6]Date: Fri 4 Feb 2005
From: Terry S. Singeltary Sr.
Source: Spongiform Encephalopathy Advisory Committee (SEAC), Position Paper, January 2005 [edited]
SNIP...
SEE FULL TEXT ;
p.s. ProMed archives are pay-per-view now. ...tss
SNIP...SEE FULL TEXT ;
cjd mother to child transmission ???
Mother passes on CJD to unborn baby
Sun, 17 Sep 2000 Telegraph By Rajeev Syal, Jenny Booth and Chris Hastings
Dr Will offers me a tour of the laboratories. As we are getting up to go, I broach something that has been bothering me. Does he think the victims will get any younger?
'Well, we now have a 12-year-old.'
A 12-year-old?
'That's what I said.'
He looks almost ashamed. Girl or boy?
'I can't say.'
But if the incubation period is at least 10 years, then the child was barely eating solid food when it contracted the infection.
'I'm not saying anything,'
the neurologist says wearily.
'You've got small children of your own, Allison. You do the maths.'
The child has been ill since she was born but tests to pinpoint the cause of the problem have so far proved inconclusive INCONCLUSIVE. What does not put an end to a thing. Inconclusive presumptions are those which may be overcome by opposing proof; for example, the law presumes that he who possesses personal property is the owner of it, but evidence is allowed to contradict this presumption, and show who is . At birth the baby, who cannot be named for legal reasons, could not swallow and was unable to gain weight.
Wednesday, December 30, 2009
Is there evidence of vertical transmission of variant CJD ?
J Neurol Neurosurg Psychiatry doi:10.1136/jnnp.2009.172148 Is there evidence of vertical transmission of variant CJD? Katy Murray (kmurray12@doctors.org.uk) + Author Affiliations NationalCJD Surveillance Unit, United Kingdom James Peters (jimmypeters1980@yahoo.co.uk) + Author Affiliations NationalCJD Surveillance Unit, United Kingdom Lesley Stellitano (lesley.stellitano@addenbrookes.nhs.uk) + Author Affiliations Addenbrooke's Hospital, United Kingdom Annemarie Winstone (annemarie.winstone@addenbrookes.nhs.uk) + Author Affiliations Addenbrooke's Hospital, United Kingdom Christopher Verity (christopher.verity@addenbrookes.nhs.uk) + Author Affiliations Addenbrooke's Hospital, United Kingdom Robert Will (r.g.will@ed.ac.uk) + Author Affiliations NationalCJD Surveillance Unit, United Kingdom Published Online First 27 April 2009
Abstract Objectives:
The possibility of vertical transmission of variant CJD (vCJD) has been raised, because of the widespread distribution of infectivity in vCJD and the demonstration that this condition can be transmitted through blood transfusion. The aim is to search for evidence of this type of transmission of vCJD. Methods: A national surveillance system for CJD has been established in the UK since 1990. Through this register details were extracted of all children born to vCJD cases up to March 2009. This list was checked against the CJD register and cases identified through the UK study of progressive intellectual and neurological deterioration in children (PIND) to determine whether any of the children of vCJD cases had themselves developed a progressive neurological disorder or vCJD.
Results: 125 children have been born to parents with a diagnosis of vCJD. Nine of these children were born to females with vCJD who were symptomatic at conception, birth or within a year of clinical onset. Only one woman was known to have breast fed her child. None of the children of vCJD cases have been referred to the NCJDSU as suspected vCJD and none have been classified as suffering from a progressive neurodegenerative disorder through the PIND study. One of the children has been investigated by the National Prion Unit (see accompanying case report). Interpretation: To date there is no evidence of vertical transmission of vCJD. However, the incubation period through this mechanism might be prolonged and it will be many years before observational data can exclude this possibility.
snip...see more here ;
Wednesday, December 30, 2009
Is there evidence of vertical transmission of variant CJD ?
BSE Inquiry DFA's a review BSE Inquiry DFA's a review
BSE Inquiry
Sunday, May 18, 2008 BSE, CJD, and Baby foods (the great debate 1999 to 2005)
TUESDAY, AUGUST 1, 2017
BSE INQUIRY DFA 17 Medicines and medical devices
Sunday, May 18, 2008
MAD COW DISEASE BSE CJD CHILDREN VACCINES
MONDAY, MAY 19, 2008
SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS
THURSDAY, JULY 22, 2010
BSE INQUIRY DFA 18 COSMETICS
Sunday, May 18, 2008
BSE Inquiry DRAFT FACTUAL ACCOUNT DFA
BSE Inquiry DRAFT FACTUAL ACCOUNTS DFA's
DFA 15 Monitoring and Enforcement of the SBO Specified Bovine Offal Regulations
SATURDAY, AUGUST 26, 2017
DFA 14 Consideration of the Risk from Mechanically Recovered Meat (MRM) in 1989-1990
BSE INQUIRY DFA 16 MID 1995 TO THE FINAL DAYS
BSE INQUIRY DFA
Singeltary communication statement to BSE Inquiry 1998
this is all in the world those 300k+ bovine that died with BSE were consuming, a nutritional supplement with srms, i.e. specified risk materials, the most highest risk tissue for the tse prion.
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100
3 July 1998 Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.net Ref: E2979
Dear Mr Singeltary,
Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died.
As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments.
Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD. I would refer you to the transcripts of evidence we have already heard which are found on our internet site at http://www.bse.org.uk. Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on 0171 261 8332 should you have any queries.
Yours sincerely Patricia Cantos Families Team Leader Attachments TSS
==============
-------- Original Message --------
Subject: re: METABOLIFE AND TSEs GAO-03-494 ''URGENT DATA''
Date: Thu, 01 May 2003 16:04:35 -0400
From: "Marcia G Crosse"
To: CC: "Charles W Davenport" , "Carolyn Feis Korman" , "Martin Gahart"
Mr. Singletary,
We were informed by representatives of Metabolife, Inc. that Metabolife 356 was reformulated to remove bovine complex as an ingredient in the product, approximately September 2001. We did not independently verify the contents of the product.
Sincerely, Marcia Crosse Acting Director Health CarePublic Health and Science Issues U.S. General Accounting Office 441 G Street, N.W. Washington, D.C. 20548
===================
snip...
TUESDAY, MAY 11, 2021
A Unique Presentation of Creutzfeldt-Jakob Disease in a Patient Consuming Deer Antler Velvet
Conclusion
We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.
Supplemental data including molecular tissue sample analysis and autopsy findings could yield further supporting evidence. Given this patient’s clinical resemblance to CBD and the known histological similarities of CBD with CJD, clinicians should consider both diseases in the differential diagnosis of patients with a similarly esoteric presentation. Regardless of the origin of this patient’s disease, it is clear that the potential for prion transmission from cervids to humans should be further investigated by the academic community with considerable urgency.
''We believe that our patient’s case of CJD is highly suspicious for cervid etiology given the circumstances of the case as well as the strong evidence of plausibility reported in published literature. This is the first known case of CJD in a patient who had consumed deer antler velvet. Despite the confirmed diagnosis of CJD, a causal relationship between the patient’s disease and his consumption of deer antler velvet cannot be definitively concluded.''
ABOUT that deer antler spray and CWD TSE PRION...
I have been screaming this since my neighbors mom died from cjd, and she had been taking a supplement that contained bovine brain, bovine eyeball, and other SRMs specified risk materials, the most high risk for mad cow disease.
just saying...
I made a submission to the BSE Inquiry long ago during the BSE Inquiry days, and they seemed pretty interested.
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100
3 July 1998
Mr Terry S Singeltary Sr.
E-Mail: Flounder at wt.net
Ref: E2979
Dear Mr Singeltary,
Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments.
Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died.
As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments.
Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD. I would refer you to the transcripts of evidence we have already heard which are found on our internet site at ;
Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it?
In the meantime, thank you for you comments. Please do not hesitate to contact me on...
snip...end...tss
everyone I tell this too gets it screwed up...MY MOTHER WAS NOT TAKING THOSE SUPPLEMENTS IPLEX (that I ever knew of). this was my neighbors mother that died exactly one year _previously_ and to the day of sporadic CJD that was diagnosed as Alzheimer’s at first. my mother died exactly a year later from the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD, and exceedingly rare strains of the ever growing sporadic CJD’s. _both_ cases confirmed. ...kind regards, terry
TSEs i.e. mad cow disease's BSE/BASE and NUTRITIONAL SUPPLEMENTS
IPLEX, mad by standard process;
vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach.
also;
what about potential mad cow candy bars ?
see their potential mad cow candy bar list too...
THESE are just a few of MANY of just this ONE COMPANY...TSS
snip...
snip...end
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
11:50 AM
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