My Photo
Name:
Location: BACLIFF, Texas, United States

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

Thursday, March 01, 2012

Variant Creutzfeldt-Jakob disease Fact sheet N°180 Revised February 2012 W.H.O.

Variant Creutzfeldt-Jakob disease

Fact sheet N°180 Revised February 2012

Key facts


--------------------------------------------------------------------------------


Variant Creutzfeldt-Jakob disease (vCJD) is a rare and fatal human neurodegenerative condition. The consumption of food of bovine origin contaminated with the agent of Bovine Spongiform Encephalopathy (BSE), a disease of cattle, has been strongly linked to the occurrence of vCJD in humans. 175 cases of vCJD were reported in the United Kingdom of Great Britain and Northern Ireland (United Kingdom), and 49 cases in other countries from October 1996 to March 2011. Following the successful containment of the BSE epidemic in cattle, the number of cases of vCJD in the United Kingdom has declined since 2000.


--------------------------------------------------------------------------------


Variant Creutzfeldt-Jakob disease (vCJD) is a rare and fatal human neurodegenerative condition which is classified as a Transmissible Spongiform Encephalopathy (TSE) because of its ability to be transmitted and the characteristic spongy degeneration of the brain that it causes.

vCJD was first described in the United Kingdom in March 1996 and has been linked with exposure to a TSE of cattle called Bovine Spongiform Encephalopathy (BSE), also known as Classical BSE1, which was first reported in the United Kingdom in 1986.

Total cases

From October 1996 to March 2011, 175 cases of vCJD have been reported in the United Kingdom, 25 in France, 5 in Spain, 4 in Ireland, 3 each in the Netherlands and the United States of America (USA), 2 each in Canada, Italy and Portugal, and one each in Japan, Saudi Arabia and Taiwan. The number of cases of vCJD in the United Kingdom peaked in 2000 with 28 deaths. It has since declined to about 2 diagnosed cases and 2 deaths per year in 2008.

Epidemiology

Before the identification of vCJD, Creutzfeldt-Jakob disease (CJD), the most common of the known human TSEs, was thought to exist in only three forms: 1.sporadic CJD, which occurs throughout the world at the rate of about one per million people, and accounts for about 85% of CJD cases; 2.familial CJD, which is associated with a gene mutation and makes up 5–15% of CJD cases; and 3.iatrogenic CJD, which results from accidental transmission via contaminated surgical equipment or as a result of corneal or meningeal (dura mater) transplants or the administration of human-derived pituitary growth hormones; this accounts for less than 5% of CJD cases. In contrast to the traditional forms of CJD, vCJD has affected younger patients (median age at death of 28 years, as opposed to 68 years) and has a relatively longer duration of illness (median of 14 months as opposed to 4.5 months).

The first person to develop symptoms of what turned out to be vCJD became ill in 1994. Most people who have developed vCJD lived in the United Kingdom. Some cases that were diagnosed in countries other than the United Kingdom occurred in people who were probably exposed to the BSE while residing in the United Kingdom.

As of early May 2011, the CJD surveillance unit for the United Kingdom reported 172 primary cases of vCJD, and three secondary cases of vCJD related to blood transfusion. Among primary cases, there are four additional cases in the United Kingdom and one in Canada where vCJD is strongly suspected, but the diagnosis has not yet been definitively confirmed by post mortem analysis.

Clinical features

Early in the illness, patients usually experience psychiatric or sensory symptoms, which most commonly take the form of depression, apathy or anxiety, and occasionally (in a third of the cases) unusual persistent and painful sensory symptoms. Neurological signs, including unsteadiness, difficulty walking and involuntary movements, develop as the illness progresses and, by the time of death, patients become completely immobile and mute.

Diagnosis The clinical presentation, progressive nature of the disease and failure to find any other diagnosis are characteristic of vCJD. There are no completely reliable tests to use before the onset of clinical symptoms. However, magnetic resonance scans and tonsillar biopsy are useful diagnostic tests. The brainwave pattern observed during an electroencephalogram is abnormal in most vCJD patients. Currently, the diagnosis of vCJD can only be confirmed following pathological examination of the brain post mortem. Characteristically, multiple microscopic and abnormal aggregates encircled by holes are seen in the brain tissue, resulting in a daisy-like appearance described by the term "florid plaques". Probable cause

The nature of the vCJD agent is being investigated and is still a matter of debate. One prevalent theory is that the agent is composed largely, if not entirely, of a self-replicating misfolded protein, referred to as a prion.

There is strong scientific evidence that vCJD is linked with exposure to a TSE of cattle called BSE. The link between vCJD and BSE was first hypothesized because of the association of these two TSEs in time and place. In addition, laboratory evidence indicates that vCJD is linked causally with BSE.

Intensive surveillance in European countries has confirmed the high incidence of vCJD in the United Kingdom, the country with the largest potential exposure to BSE. Several cases in other countries were likely exposed to the BSE agent while residing in the United Kingdom.

The most likely cause of vCJD is exposure to the BSE agent through consumption of food from bovine origin most plausibly contaminated by infected bovine brain or other central nervous system tissue.

Only four cases of vCJD infection have been associated with blood transfusion: three of these cases developed symptoms of vCJD several years after transfusion, and one died from unrelated causes before developing symptoms of vCJD, but was shown to be infected with vCJD.

Measures taken to protect public health Due to the strong evidence of a link between vCJD and BSE, the UK government made BSE a notifiable disease in 1988. Since 1994, the European Union has progressively implemented control measures that have contained BSE. The main measures are detailed in the information sheet on Bovine Spongiform Encephalopathy. Since 1999, the United Kingdom has no longer sourced plasma from its inhabitants, and as a further precautionary measure against the occurrence of vCJD, has instituted leukocyte depletion (removal of white blood cells) from blood transfusions. Some countries have prohibited donations of blood from persons who have resided in countries with higher risk of BSE.

WHO response

WHO has worked on: convening scientific consultations on issues related to animal and human TSEs (these meetings have made recommendations aimed at protecting human and animal health); assisting with global surveillance of CJD and its variants, by holding training courses worldwide, particularly in developing countries, to help countries establish national surveillance of CJD and its variants; convening the Technical Consultation on BSE: Public Health, Animal Health and Trade, publishing the WHO manual for surveillance of human transmissible spongiform encephalopathies, including variant Creutzfeldt-Jakob disease. WHO recommendations

To protect human health, WHO has several recommendations. No tissue that is likely to contain the BSE agent, nor part or product of any animal which has shown signs of a TSE should enter the (human or animal) food chain. All countries should ban the use of ruminant tissues in ruminant feed. The pharmaceutical industry should avoid the use of bovine materials and materials from other animal species in which TSEs naturally occur. If their use is absolutely necessary, these materials should be obtained from countries which have a surveillance system for BSE in place and which reports zero cases of BSE. The Guidelines on tissue infectivity distribution in transmissible spongiform encephalopathies in 2006 provide information and assist national regulatory authorities in conducting risk assessments of vCJD transmission. In 2010, WHO updated the Tables on tissue infectivity distribution in transmissible spongiform encephalopathies. The Tables reflect the current status of knowledge about infectivity in body tissues, secretions, and excretions of humans and animals, and thus provide information about potential transmission of vCJD through human blood and blood products, as well as through medicinal products prepared with animal-derived materials.


--------------------------------------------------------------------------------


1 The term "Classical BSE" has been introduced to differentiate the disease from Atypical BSE cases, which occur rarely in the cattle population.



http://www.who.int/mediacentre/factsheets/fs180/en/




WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010


http://www.who.int/bloodproducts/tablestissueinfectivity.pdf





Key facts missed ;




Monday, October 10, 2011


EFSA Journal 2011 The European Response to BSE: A Success Story

snip...

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip...



http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1





http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf






see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;



http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html







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






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







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







Saturday, June 25, 2011


Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque


"BSE-L in North America may have existed for decades"



http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html







Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.


snip...


The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...



http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf






Sunday, February 5, 2012


February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE


http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/february-2012-update-on-feed.html







PLEASE STUDY THIS MAP !




SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS. ...TSS





http://wwwnc.cdc.gov/eid/article/18/3/11-0685-f1.htm







*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***





Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012




http://wwwnc.cdc.gov/eid/ahead-of-print/article/18/3/11-0685_article.htm








Thursday, February 09, 2012


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE


http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html







Wednesday, February 15, 2012


New Supplement from Deer Antler Velvet, CWD, and CJD there from ?


New Deer Antler Velvet Extract Changes the World of Supplements


http://chronic-wasting-disease.blogspot.com/2012/02/new-supplement-from-deer-antler-velvet.html






Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Sheep Naturally/Experimentally Infected with Scrapie and Deer with Preclinical/Clinical Chronic Wasting Disease▿


Richard Rubenstein1,*,
Binggong Chang1,
Perry Gray2,
Martin Piltch2,
Marie S. Bulgin3,
Sharon Sorensen-Melson3 and
Michael W. Miller4
+ Author Affiliations



1Departments of Neurology and Physiology/Pharmacology, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, New York 11203

2Los Alamos National Laboratory, Los Alamos, New Mexico 87545

3University of Idaho, Caine Veterinary Teaching and Research Center, 1020 E. Homedale Road, Caldwell, Idaho 83607

4Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, Colorado 80526-2097



ABSTRACT



Prion diseases, also known as transmissible spongiform encephalopathies, are fatal neurodegenerative disorders. Low levels of infectious agent and limited, infrequent success of disease transmissibility and PrPSc detection have been reported with urine from experimentally infected clinical cervids and rodents. We report the detection of prion disease-associated seeding activity (PASA) in urine from naturally and orally infected sheep with clinical scrapie agent and orally infected preclinical and infected white-tailed deer with clinical chronic wasting disease (CWD). This is the first report on PASA detection of PrPSc from the urine of naturally or preclinical prion-diseased ovine or cervids. Detection was achieved by using the surround optical fiber immunoassay (SOFIA) to measure the products of limited serial protein misfolding cyclic amplification (sPMCA). Conversion of PrPC to PrPSc was not influenced by the presence of poly(A) during sPMCA or by the homogeneity of the PrP genotypes between the PrPC source and urine donor animals. Analysis of the sPMCA-SOFIA data resembled a linear, rather than an exponential, course. Compared to uninfected animals, there was a 2- to 4-log increase of proteinase K-sensitive, light chain immunoglobulin G (IgG) fragments in scrapie-infected sheep but not in infected CWD-infected deer. The higher-than-normal range of IgG levels found in the naturally and experimentally infected clinical scrapie-infected sheep were independent of their genotypes. Although analysis of urine samples throughout the course of infection would be necessary to determine the usefulness of altered IgG levels as a disease biomarker, detection of PrPSc from PASA in urine points to its potential value for antemortem diagnosis of prion diseases.



FOOTNOTES

Received 13 May 2011.

Accepted 14 June 2011.

↵*Corresponding author. Mailing address: Downstate Medical Center, Departments of Neurology and Physiology/Pharmacology, Box 1213, 450 Clarkson Avenue, Brooklyn, NY 11203. Phone: (718) 270-2019. Fax: (718) 270-2459. E-mail: richard.rubenstein@downstate.edu.

↵▿ Published ahead of print on 29 June 2011.


Copyright © 2011, American Society for Microbiology. All Rights Reserved.



http://jvi.asm.org/content/85/17/9031.abstract






Thursday, June 09, 2011

Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission


http://chronic-wasting-disease.blogspot.com/2011/06/detection-of-cwd-prions-in-salivary.html






Wednesday, March 18, 2009

Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay


http://chronic-wasting-disease.blogspot.com/2009/03/detection-of-cwd-prions-in-urine-and.html






Monday, November 30, 2009


USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE


http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html






Thursday, February 23, 2012


Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012


http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/atypical-scrapie-nor-98-confirmed.html






BSE: TIME TO TAKE H.B. PARRY SERIOUSLY


If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...


http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf






ONE HUNDRED AND FOURTEENTH ANNUAL MEETING of the United States Animal Health Association


White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection


Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS


Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheepderived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.






http://www.usaha.org/Portals/6/Proceedings/USAHAProceedings-2010-114th.pdf







Tuesday, February 14, 2012


White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease


http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/white-house-budget-proposes-cuts-to-ag.html






Thursday, February 16, 2012


Bovine Spongiform Encephalopathy BSE


31 USA SENATORS ASK PRESIDENT OBAMA TO HELP SPREAD MAD COW DISEASE 2012


http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/bovine-spongiform-encephalopathy-bse-31.html






Thursday, February 23, 2012


EIGHT FORMER SECRETARIES OF AGRICULTURE SPEAKING AT USDA'S 2012 AGRICULTURE OUTLOOK FORUM INDUCTED INTO USA MAD COW HALL OF SHAME


http://madcowusda.blogspot.com/2012/02/eight-former-secretaries-of-agriculture.html






Sunday, February 12, 2012


National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas


snip...


CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER




Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas




Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas. She left 6 Kids and a Husband. The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.-




Physician Discharge Summary, Parkland Hospital, Dallas Texas




Admit Date: 12/29/2009 Discharge Date: 1/20/2010 Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General Neurology Team



snip...




The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically. Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.




snip...



http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8







>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<



SEE MORE HERE ;


CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER






http://cjdtexas.blogspot.com/2010/03/cjd-texas-38-year-old-female-worked.html






snip...



see ;



Sunday, February 12, 2012



National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas



http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html







Wednesday, November 09, 2011


Case report Sporadic fatal insomnia in a young woman: A diagnostic challenge: Case Report TEXAS



HOW TO TURN A POTENTIAL MAD COW VICTIM IN THE USA, INTO A HAPPENSTANCE OF BAD LUCK, A SPONTANEOUS MUTATION FROM NOTHING.



OR WAS IT $$$



http://creutzfeldt-jakob-disease.blogspot.com/2011/11/case-report-sporadic-fatal-insomnia-in.html







Creutzfeldt-Jakob Disease Surveillance in Texas


http://cjdtexas.blogspot.com/2010/06/usa-cases-of-dpcjd-rising-with-24-cases.html






Sunday, July 11, 2010


CJD or prion disease 2 CASES McLennan County Texas population 230,213 both cases in their 40s


http://creutzfeldt-jakob-disease.blogspot.com/2010/07/cjd-2-cases-mclennan-county-texas.html





http://cjdtexas.blogspot.com/





see the continuing rise of sporadic CJD in Texas here ;


http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/data/






Saturday, March 5, 2011


MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA


http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html






Sunday, August 21, 2011

The British disease, or a disease gone global, The TSE Prion Disease


(see video here)


http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html





U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ?


(see video at bottom)


http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html





Sunday, September 6, 2009


MAD COW USA 1997


(SEE SECRET VIDEO)


http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html






Wednesday, June 15, 2011


Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor


http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html









Tuesday, November 08, 2011

Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011

Original Paper

Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.


http://creutzfeldt-jakob-disease.blogspot.com/2011/11/can-mortality-data-provide-reliable.html






Friday, November 04, 2011

Diagnostic accuracy of cerebrospinal fluid protein markers for sporadic Creutzfeldt-Jakob disease in Canada: a 6-year prospective study Research article


http://creutzfeldt-jakob-disease.blogspot.com/2011/11/diagnostic-accuracy-of-cerebrospinal.html






Monday, September 26, 2011

Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS, gCJD, hvCJD, sCJD, TSE, PRION, update 2011


http://prionopathy.blogspot.com/2011/09/variably-protease-sensitive-prionopathy.html






Monday, June 27, 2011


Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease


http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html





Thursday, July 10, 2008

A New Prionopathy update July 10, 2008


http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html





Thursday, July 10, 2008

A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008 Friday, June 20, 2008


http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.html





Sunday, August 10, 2008

A New Prionopathy OR more of the same old BSe and sporadic CJD


http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html





Sunday, August 24, 2008

Sporadic Fatal Insomnia with Unusual Biochemical and Neuropathological Findings


http://sporadicffi.blogspot.com/2008/08/sporadic-fatal-insomnia-with-unusual.html





Here we go folks. AS predicted. THIS JUST OUT ! as i predicted, more BSe. ...



Tuesday, August 03, 2010

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein


http://creutzfeldt-jakob-disease.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html






Monday, August 9, 2010


Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?


snip...see full text ;


http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/variably-protease-sensitive-prionopathy.html





http://prionopathy.blogspot.com/2011/05/variably-protease-sensitive-prionopathy.html





O.K. let's compare some recent cases of this prionpathy in other countries besides Gambetti's first 10 recently, that he claims is a spontaneous event, from a genetic disorder, that is not genetic, but sporadic, that is related to no animal TSE in North America, or the world. ...



http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html







http://prionopathy.blogspot.com/





http://prionpathy.blogspot.com/





http://sporadicffi.blogspot.com/






Sunday, August 09, 2009


CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009


http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html






Tuesday, August 18, 2009



BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009



http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html







LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.

This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$

ALABAMA MAD COW g-h-BSEalabama

In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.



http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156





http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF






Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY



(see mad cow feed in COMMERCE IN ALABAMA...TSS)


http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html





her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).


This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.

Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA

NATURE|Vol 457|26 February 2009


http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html






Thursday, June 23, 2011

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits


http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html






Thursday, July 21, 2011

A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:

August 2011 - Volume 70 - Issue 8 - pp 698-702


http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html








Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

USDA BSE SURVEILLANCE AND TESTING: A FAILED BROKE SYSTEM


http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html








layperson



Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net

Labels:

0 Comments:

Post a Comment

Subscribe to Post Comments [Atom]

Links to this post:

Create a Link

<< Home