SEE these further comments, this time from the CDC on this CJD case. Seems they are oblivious. ...TSS
----- Original Message -----
From: Hammett, Teresa (CDC/OID/NCZVED)
Sent: Monday, May 24, 2010 11:10 AM
Subject: RE: TO CDC - INQUIRY ABOUT vCJD DEATH OF SLAUGHTER HOUSE WORKER IRMA LINDA ANDABLO
Dear Ms Shields,
We are not able to confirm knowledge of a specific CJD investigation or diagnosis for anyone due to reasons of confidentiality. I can tell you that all persons suspected of having CJD who are less than 55 years of age are a high priority for investigation by state health departments, CDC and the National Prion Disease Pathology Surveillance Center.
There are multiple surveillance methods in place to identify cases of CJD and variant CJD when such cases occur in the United States. The CDC monitors the trends and current incidence of CJD in the United States using several surveillance mechanisms. On a routine basis, CDC reviews the national multiple cause-of-death data taken from death certificates and compiled by the National Center for Health Statistics, CDC. In addition, CDC conducts follow-up review of clinical and neuropathology records of CJD decedents aged <55 years who are identified through the national mortality data analysis or reported by health care workers. This is the age group in which almost all of the vCJD cases worldwide have occurred to date. In 1996-97, CDC established, in collaboration with the American Association of Neuropathologists, the National Prion Disease Pathology Surveillance Center at Case Western Reserve University, which performs special state-of-the-art diagnostic tests for prion diseases, including post-mortem tests for vCJD. These tests are provided free of charge to all U.S. physicians. For more information about the center, visit its website at: http://www.cjdsurveillance.com. Currently, CDC works with selected state health departments on various enhanced CJD surveillance projects and education programs regarding the importance of autopsy to both the surveillance and diagnosis of CJD. In addition, CDC collects, reviews and when indicated, actively investigates specific reports by health care personnel or institutions in all states of possible iatrogenic CJD and variant CJD cases. Three cases of vCJD have been reported from the United States. By convention, variant CJD cases are ascribed to the country of initial symptom onset, regardless of where the exposure occurred. There is strong evidence that suggests that two of the three cases were exposed to the BSE agent in the United Kingdom and that the third was exposed while living in Saudi Arabia. Cases of classic CJD in persons less than 55 years of age do occur as either sporadic cases or due to inherited mutations of the prion protein gene. Classic CJD has nothing to do with exposure to beef as does variant CJD.
From: Helane Shields[SMTP:HSHIELDS@WORLDPATH.NET]
Sent: Friday, May 21, 2010 8:17:38 PM
To: NCID DVRD PRION (CDC)
Subject: TO CDC - INQUIRY ABOUT vCJD DEATH OF SLAUGHTER HOUSE WORKER IRMA LINDA ANDABLO Auto forwarded by a Rule
To CDC - Please advise if you have investigated or conducted an autopsy regarding the CJD or vCJD death of 38 year old slaughterhouse worker Irma Linda Andablo: I originally made this inquiry to USDA. They advised it should be directed to you. Please comment or state the position of the CDC with regard to the recent death of a 38-year old long time slaughterhouse worker from variant Creutzfeldt Jakob Disease ?
CDC STATED THAT ;
"Cases of classic CJD in persons less than 55 years of age do occur as either sporadic cases or due to inherited mutations of the prion protein gene. Classic CJD has nothing to do with exposure to beef as does variant CJD."
This is wrong. It has never been proven that 85% to 90% of all cases of human TSE i.e. sporadic Creutzfeldt Jakob Disease (CJD) is of a ''inherited mutations of the prion protein gene" and or that "Classic CJD has nothing to do with exposure to beef as does variant CJD", this is simply wishful thinking$
There is much more to this nightmare than the UKBSEnvCJD hamburger eating adolescents only theory. WE are missing the bigger picture, i.e. 85%+ of all the rest of the cases i.e. sporadic Creutzfeldt Jakob Disease, and all it's phenotypes, and they are mounting. sporadic CJD is NOT a single strain, but multiple strains of UNKNOWN origin. There are six documented strains of sporadic CJD, with UNKNOWN strains growing. please remember ;
USA sporadic CJD cases rising ;
18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.
64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.
3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse Models
Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University
Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years.
***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.***
6:30 Close of Day One
SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ...
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection. He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
2008 - 2010 The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
CJD USA RISING, with UNKNOWN PHENOTYPE ; 5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.
Saturday, January 2, 2010 Human Prion Diseases in the United States January 1, 2010 ***FINAL***
my comments to PLosone here ;
CJD RISING SWITZERLAND
CJD is a predominantly sporadic disorder but can also occur as a dominantly inherited or infective condition. Only one of the 26 most recent confirmed cases was identified as carrying a disease related mutation of the PRNP gene, none had identifiable iatrogenic exposure, and none resembled variant CJD. Thus 25 of the 26 cases appear to be sporadic cases. Sporadic CJD is distributed worldwide with a reported incidence of about one in a million per year. Raised awareness of the disease in recent years could account for an increase in reported cases of CJD, although neither an increase in the average age of patients nor more frequent recognition of CJD amongst residents of nursing homes (where dementing illness is prevalent and misdiagnosis might be expected) were seen in the Swiss cases. Moreover, improved ascertainment as an explanation for the observed increase would imply levels of under-reporting in countries other than Switzerland, which appear implausible. The authors of the Lancet report suggest that the rise in cases might be due to some form of unidentified iatrogenic transmission or to exposure to a zoonotic source of infection, though cases do not resemble variant Creutzfeldt-Jakob disease (vCJD). The ongoing surveillance of CJD in Switzerland and the rest of Europe is essential to monitor the situation to see if this rise is sustained in Switzerland, and if a similar rise occurs in other countries (see http://www.eurocjd.ed.ac.uk).
Prion data suggest BSE link to sporadic CJD Declan Butler Predicting the number of cases of Creutzfeldt–Jakob disease (CJD) in people as a result of transmission of bovine spongiform encephalopathy (BSE) has just got more difficult.Whereas it was thought that BSE only caused a new form of the disease called variant CJD (vCJD), a study in mice from a team led by John Collinge at University College London suggests that it may also cause a disease indistinguishable from the commonest form of classical, or 'sporadic', CJD (E.
IF we look at sporadic incidence of CJD in UK from 1993 to 2003, the incidence rose from 37 in 1993 to 77 in 2003. THIS seems to show an increase to me? I do not understand the statement ; However, in the period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of U.K. sporadic CJD deaths (52). IF we go further and look at some of the other documented BSE countries, you will the increase of sporadic CJD there as well ;
Canada from 2 to 25
France from 35 to 108
Germany 21+ to 96
Italy 27 to 76
Switzerland sporadic CJD ;
Swiss rise in CJD raises concerns over possible BSE link [LONDON] THE LANCET Plaque attack: Swiss patients have spongiform patterns in the brain typical of sporadic CJD. The number of people dying from Creutzfeldt-Jakob disease (CJD) has risen sharply in Switzerland -- sparking fears of a possible link with bovine spongiform encephalopathy (BSE). BSE is thought to be the cause of a distinctive form of the brain-wasting disease known as variant CJD. The Swiss cases, in contrast, are standard 'sporadic' CJD. Each year between 1997 and 2000, no more than 11 Swiss people developed CJD. But 19 cases were reported in 2001, and seven were recorded in the first quarter of this year. This is some four times higher than the incidence elsewhere, reports a team led by Adriano Aguzzi of the University Hospital Zurich (M. Glatzel et al. Lancet 360, 139-141; 2002). The increase could be a mere statistical blip, or it may be due to increased awareness of the disease leading to more diagnoses. More disturbing is the possibility that the cases are linked to the consumption of BSE-infected meat products -- which would mean that the BSE agent can cause two distinct forms of CJD. Possible links between the Swiss CJD cases and BSE will now be explored by strain-typing experiments in which the disease is transmitted to mice. These tests will take at least a year to complete. "It's the best way to establish or exclude any suspected link," says Moira Bruce of the UK Institute for Animal Health's Neuropathogenesis Unit in Edinburgh.
Experiences in England and Switzerland -- two countries that discovered mad cow disease in their cattle -- have heightened concerns about the possibility some cases of sporadic CJD are due to consuming mad-cow-tainted beef. Both countries have reported increases in sporadic CJD since mad cow was first detected in British herds in 1986. Switzerland discovered last year its CJD rate was twice that of any other country in the world. Switzerland had been seeing about eight to 11 cases per year from 1997 to 2000. Then the incidence more than doubled, to 19 cases in 2001 and 18 cases in 2002.
Mouse model sheds new light on human prion disease snip... Professor John Collinge said We are not saying that all or even most cases of sporadic CJD are as a result of BSE exposure, but some more recent cases may be the incidence of sporadic CJD has shown an upward trend in the UK over the last decade. While most of this apparent increase may be because doctors are now more aware of CJD and better at diagnosing it, serious consideration should be given to a proportion of this rise being BSE-related. Switzerland, which has had a substantial BSE epidemic, has noted a sharp recent increase in sporadic CJD.
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth, and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: email@example.comReceived August 1, 2002; Revised September 24, 2002; Accepted October 17, 2002. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/?tool=pubmed The EMBO Journal (2002) 21, 6358 - 6366 doi:10.1093/emboj/cdf653
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante1, Jacqueline M. Linehan1, Melanie Desbruslais1, Susan Joiner1, Ian Gowland1, Andrew L. Wood1, Julie Welch1, Andrew F. Hill1, Sarah E. Lloyd1, Jonathan D.F. Wadsworth1 and John Collinge1 1.MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK Correspondence to: John Collinge, E-mail: firstname.lastname@example.org Received 1 August 2002; Accepted 17 October 2002; Revised 24 September 2002
Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure. Keywords:BSE, Creutzfeldt–Jakob disease, prion, transgenic
Sunday, August 10, 2008
A New Prionopathy OR more of the same old BSe and sporadic CJD
CJD IN INDIVIDUAL WITH BSE HERD WHOM DRANK MILK THERE FROM (rewriting history)
CONFIDENTIAL CONFIRMED CASE OF CJD IN A DAIRY FARMER
3. Neither Dr Will nor the CJD surveillance unit intend to disclose the existence of this case or make any comment at present unless it attracts media attention.
HUMAN CASE DETAILS CONFIDENTIAL
6. CJD IN FARMERS
The second annual report on CJD surveillance in the UK, which is about to be published, gives occupational history details of 29 definite and probable CJD cases recorded in people who had a history of employment at any time in particular occupational groups of potential significance for the occurrence of the disease. The 29 cases were amongst 95 diagnosed over a 3 year period: the other 66 cases did not fall into such occupational groups. These relevant details are:- MEDICAL/PARAMEDICAL/DENTISTRY 7 ANIMAL LABORATORY 1 PHARMACEUTICAL LABORATORY 0 RESEARCH LABORATORY 0 FARMERS/VETERINARY SURGEONS 7 BUTCHERS/ABATTOIR WORKERS/OCCUPATION INVOLVING DIRECT CONTACT WITH ANIMAL OR CARCASES 5 OCCUPATION INVOLVING ANIMAL PRODUCTS 9
snip... full text ;
Over a 5 year period, which is the time period on which the advice from Professor Smith and Dr. Gore was based, and assuming a population of 120,000 dairy farm workers, and an annual incidence of 1 per million cases of CJD in the general population, a DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN an individual in the general population to develop CJD. Using the actual current annual incidence of CJD in the UK of 0.7 per million, this figure becomes 7.5 TIMES. 3. You will recall that the advice provided by Professor Smith in 1993 and by Dr. Gore this month used the sub-population of dairy farm workers who had had a case of BSE on their farms - 63,000, which is approximately half the number of dairy farm workers - as a denominator. If the above sums are repeated using this denominator population, taking an annual incidence in the general population of 1 per million the observed rate in this sub-population is 10 TIMES, and taking an annual incidence of 0.7 per million, IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than that in the general population...
4th farmer, and 1st teenager
CHANGING SCIENCE TO FIT YOUR INDUSTRY NEEDS COVER-UP IN FULL MODE NOW
PROBLEM 7. The main findings in the case-control study were STATISTICALLY SIGNIFICANT ASSOCIATIONS BETWEEN CONSUMPTION OF VEAL OR VENISON AND THE DEVELOPMENT OF CJD (INCREASED RISKS OF 2-13x). IP PS(L) wishes to probe this further we think it best to explain the matter VERBALLY. The problem is how to present the findings in this year's annual report in a way which avoids unnecessary public alarm and limits the scope for media scare stores. (or the facts...TSS)
A REVISED VERSION WHERE THE FOLLOWING WAS MADE TO BE REMOVED FROM SCIENTIFIC FINDINGS. ...TSS
''This year's findings show a number of associations but the strongest is for veal.'' A BIG LINE WAS DRAWN THROUGH THAT SENTENCE TO BE REMOVED DUE TO THE FOLLOWING. THIS IS THE NEXT SENTENCE ; ''This is of considerable concern given recent developments. In particular, Ministers will be particularly concerned about the European dimension given the recent troubles with the Germans.'' YOU can see the beginning of the ukbsenvCJD only theory beginning to unfold now.
full text of this ukbsenvcjd only conspiracy can be seen here. ...TSS
see full text sporadic CJD the big lie;
CJD IN AN INDIVIDUAL OCCUPATIONALLY EXPOSED TO BSE ii. on page 2 the sentence ''He had drunk pooled milk from the herd which included that from the affected animal'' will mislead the uninformed. It needs to be made clear that milk from a cow which is suspected to be affected with BSE cannot be drunk or added to the bulk milk produced by the rest of the herd. iii. in the final paragraph I suggest that the phrase ''and a causal link with BSE is at most conjectural'' BE DELETED: the first paragraph of the sentence would then stand as a clear statement that the CJD case was likely to have been a CHANCE PHENOMENON.
''DH is aware of a second case of CJD in a dairy farmer who has had BSE in his herd. We cannot comment on the details of the case, but we know of nothing to suggest this is anthing other than a sporadic case of CJD. .........
IF PRESSED: The numbers concerned are very small, and it is not possible to draw any conclusions from such small numbers. This issue is being considered by the Government's expert advisers....
THE FARMER IS THOUGHT TO HAVE HAD AT LEAST TWO CASES OF BSE IN HIS HERD, which were diagnosed in 1992. The farmer is reported to have asssisted in calving and to have drunk milk from his herd. This does not suggest that this is anything other than a sporadic case of CJD. ...
CONFIRMED CASE OF CJD IN DAIRY FARMER The Committee agreed that transmission studies in relation to ''the third farmer'' with potential occupational contact with BSE was a priority. ....
3RD FARMER BSE CJD TRANSMISSION STUDIES MRC
CJD FARMERS WIFE 1989
Locally, they made quite an association with BSE, since she was a farmers wife on a farm that, atypically for that area of S Yorkshire, had several BSE cases. I was told the clinical and pathological pictures were typical of CJD.
cover-up of 4th farm worker ???
RISTRICTED: POLICY 23 October 1995
CONFIRMATION OF CJD IN FOURTH FARMER
now story changes from; SEAC concluded that, if the fourth case were confirmed, it would be worrying, especially as all four farmers with CJD would have had BSE cases on their farms. to; This is not unexpected... was another farmer expected?
Monday, May 19, 2008 SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010
(special pre-congress edition)
18.173 page 189
Experimental Challenge of Cattle with H-type and L-type Atypical BSE
A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada
Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.
Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.
Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types.
Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.
14th ICID International Scientific Exchange Brochure - Final
Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary Bacliff, TX, USA
Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods: 12 years independent research of available data
Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
International Society for Infectious Diseases Web:
Sunday, February 14, 2010
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE?
'' Professor Kong reply ;
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE
Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden
Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.
Archive Number 20100405.1091 Published Date 05-APR-2010 Subject PRO/AH/EDR> Prion disease update 1010 (04)
[Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
Prions: Protein Aggregation and Infectious Diseases
ADRIANO AGUZZI AND ANNA MARIA CALELLA Institute of Neuropathology, University Hospital of Zurich, Zurich, Switzerland
3. Sporadic Creutzfeldt-Jakob disease Approximately 85% of all human prion diseases are sporadic forms of CJD. For sCJD, there is no association with a mutant PRNP allele, nor is there any epidemiological evidence for exposure to a TSE agent through contact with people or animals infected with TSEs. sCJD cases are currently subclassified according to the methionine/valine polymorphism at codon 129 of the PRNP gene and the size and glycoform ratio of proteaseresistant prion protein identified on western blot (type 1 or type 2) (174). Heterozygosity (Met/Val) at PrP codon 129 appears to be associated with a lower risk (378) and/or prolonged incubation time (119, 387). The lack of routine laboratory testing for preclinical diagnosis makes the search for agent sources and other risk factors extremely difficult. At present, the means of acquisition of a TSE agent in these patients remains a mystery. So far, there is no evidence for spontaneous PrPSc formation in any animal or human TSE. In humans, the peak age incidence of sporadic CJD is 55–60 years. However, if spontaneous misfolding were the primary event, one might expect a continuously increasing incidence with age because more time would allow more opportunity for rare misfolding events.
Physiol Rev • VOL 89 • OCTOBER 2009 • www.prv.org
Perspectives BIOMEDICINE: A Fresh Look at BSE Bruce Chesebro*
Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle form of a family of progressive brain diseases. These diseases include scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and chronic wasting disease (CWD) in deer and elk. They are also known as either "prion diseases" because of the association of a misfolded cellular prion protein in pathogenesis or "transmissible spongiform encephalopathies" (TSEs) because of the spongelike nature of the damaged brain tissue (1).
The recent discovery of two BSE-infected cows, one in Canada and one in the United States, has dramatically increased concern in North America among meat producers and consumers alike over the extent to which BSE poses a threat to humans as well as to domestic and wild animals. The European BSE epidemic of the late-1980s seems to have been initiated a decade earlier in the United Kingdom by changes in the production of meat and bone meal (MBM) from rendered livestock, which led to contamination of MBM with the BSE infectious agent. Furthermore, the fact that UK farmers fed this rendered MBM to younger animals and that this MBM was distributed to many countries may have contributed to the ensuing BSE epidemic in the United Kingdom and internationally (2).
Despite extensive knowledge about the spread of BSE through contaminated MBM, the source of BSE in Europe remains an unsolved mystery (2). It has been proposed that BSE could be derived from a cross-species infection, perhaps through contamination of MBM by scrapie-infected sheep tissues (see the figure). Alternatively, BSE may have been an endemic disease in cattle that went unnoticed because of its low level of horizontal transmission. Lastly, BSE might have originated by "spontaneous" misfolding of the normal cellular prion protein into the disease-associated abnormal isoform (3), which is postulated to be the infectious agent or "prion."
Five possible sources of BSE in North American cattle. Sheep, deer, and elk could spread prion diseases (TSEs) to cattle through direct animal contact or contamination of pastures. Endemic BSE has not been proven to exist anywhere in the world, but it is difficult to exclude this possibility because of the inefficient spread of BSE infectivity between individual animals (2). BSE caused by spontaneous misfolding of the prion protein has not been proven. CREDIT: KATHARINE SUTLIFF/SCIENCE
Nevertheless, the idea that BSE might originate due to the spontaneous misfolding of prion proteins has received renewed interest in the wake of reports suggesting the occurrence of atypical BSE (9-11). These results imply that new strains of cattle BSE might have originated separately from the main UK outbreak. Where and how might such strains have originated? Although such rare events cannot be studied directly, any number of sources of the original BSE strain could also explain the discovery of additional BSE strains in cattle (see the figure). However, it would be worrisome if spontaneous BSE were really a valid etiology because such a mechanism would be impossible to prevent--unlike other possible scenarios that could be controlled by large-scale eradication of TSE-positive animals.
Another way to look at this problem is to examine evidence for possible spontaneous TSE disease in other animals besides cattle. Spontaneous BSE would be extremely difficult to detect in cattle, where horizontal spread is minimal. However, in the case of the sheep TSE disease, scrapie, which spreads from ewes to lambs at birth as well as between adults, spontaneous disease should be detectable as new foci of clinical infection. In the early 1950s scrapie was eradicated in both Australia and New Zealand, and the mainland of both these countries has remained scrapie-free ever since. This scrapie-free status is not the result of selection of sheep resistant to scrapie because sheep from New Zealand are as susceptible as their UK counterparts to experimental scrapie infection (12). These experiments of man and nature appear to indicate that spontaneous clinical scrapie does not occur in sheep. Similarly, because CWD is known to spread horizontally, the lack of CWD in the deer or elk of eastern North America but its presence in western regions would also argue against a spontaneous disease mechanism. This is particularly noteworthy in New Zealand, where there are large numbers of deer and elk farms and yet no evidence of spontaneous CWD. If spontaneous scrapie does not occur in sheep or deer, this would suggest that spontaneous forms of BSE and sporadic Creutzfeldt-Jakob disease (sCJD) are unlikely to be found in cattle or humans. The main caveat to this notion is that spontaneous disease may arise in some animal species but not others. In humans, sCJD--which is considered by some researchers to begin by spontaneous misfolding of the prion protein--usually takes more than 50 years to appear. Thus, in animals with a shorter life-span, such as sheep, deer, and cattle, an analogous disease mechanism might not have time to develop.
What can we conclude so far about BSE in North America? Is the BSE detected in two North American cows sporadic or spontaneous or both? "Sporadic" pertains to the rarity of disease occurrence. "Spontaneous" pertains to a possible mechanism of origin of the disease. These are not equivalent terms. The rarity of BSE in North America qualifies it as a sporadic disease, but this low incidence does not provide information about cause. For the two reported North American BSE cases, exposure to contaminated MBM remains the most likely culprit. However, other mechanisms are still possible, including cross-infection by sheep with scrapie or cervids with CWD, horizontal transmission from cattle with endemic BSE, and spontaneous disease in individual cattle. Based on our understanding of other TSEs, the spontaneous mechanism is probably the least likely. Thus, "idiopathic" BSE--that is, BSE of unknown etiology--might be a better term to describe the origin of this malady. ...
snip...full text ;
Release No. 0106.04
Contact: Office of Communications (202) 720-4623
Transcript of Remarks From Technical Briefing on BSE and Related Issues With Agriculture Secretary Ann M. Veneman and USDA Chief Veterinary Officer Dr. Ron DeHaven Washington D.C. - March 15, 2004
OPERATOR : “Yes. Our next one is coming from Elizabeth Weiss. Please state your company.”
ELIZABETH WEISS: “This is Elizabeth Weiss with USA Today.”
“I actually had two questions. First off, when you say you're looking for 1 in 10,000 cases, is USDA doing any work to find out the possibility of whether or not BSE exists in a spontaneous form in the way that it does in humans and elk populations?
“And secondly, how will any of this fit into some of the consternation that's been raised in California and with the Midwest packer that wanted to test all of its cattle?
DR. DEHAVEN: “All right. I think we've got three different questions in there, and I'll try to touch on each one of them.
“First of all, let me correct just a technical issue, and that is you mentioned 1 in 10,000. And actually our surveillance system currently is designed, the one that we have in place now is designed to detect 1 positive in 1 million cattle, and I gave some numbers between 200,000 and 268,000 that would allow us to detect 1 in 10 million as opposed to 1 in 10,000.
“So we would, if we were able to collect in the ballpark of those numbers of samples then we with increasing numbers of samples have an increasingly statistically valid sample from which to determine, one, whether or not the disease exists and, if so, at what prevalence level.
“So our real emphasis is to test as many of those animals as we can, ensure that we get an appropriate geographical distribution, but not setting a specific number as far as a target. Again, consistent with the recommendation from the International Review Team, their recommendation was to test all of them.
“So that's consistent with where we're going is to test as many as we possibly can.
“As far as spontaneous cases, that is a very difficult issue. There is no evidence to prove that spontaneous BSE occurs in cattle; but here again it's an issue of proving a negative. We do know that CJD, the human version of the disease, does occur spontaneously in humans at the rate of about 1 in 1 million. We don't have enough data to definitively say that spontaneous cases of BSE in cattle occur or do not occur.
“Again, it's a very difficult situation to prove a negative.
“So a lot of research is ongoing. Certainly if we do come up with any positive samples in the course of this surveillance we will be looking at that question in evaluating those samples but no scientifically hard evidence to confirm or refute whether or not spontaneous cases of BSE occur.
UK TESTING FINISHED NEXT WEEK
Matthews confirmed that the brain tissue samples from the US animal had arrived at Weybridge. Test results were likely to be ready by the end of next week, he said.
The suspect animal has already undergone a series of tests. A rapid screening test on Nov. 15 returned inconclusive results. Sophisticated immunohistochemistry (IHC) tests cleared the animal of any infection, but a third round of testing using a Western blot procedure showed a "weak positive".
Weybridge will do an IHC test plus three kinds of Western Blot tests on the samples. They will use "methods of slightly different analytical sensitivity that give us the greatest number of opportunities to interpret what we see," he said.
US beef industry leaders say scientists should not speculate about the unusual case.
"There's no evidence that it's atypical ... and there's absolutely no evidence that it's spontaneous," said Gary Weber, head of regulatory affairs at the National Cattlemen's Beef Association.
Matthews noted scientists are still grappling with what is typical and atypical BSE.
"Far too few people have looked at BSE in depth using all of the tests to be able to define 'this is normal and that one isn't'," he said.
Weber noted Japan used the term to describe two very young infected cattle because BSE is usually found in older animals. Italy labeled a case "atypical" because the misshaped prions were found in unexpected parts of the animal's brain. ...
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (TRANSCRIPT)
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
Friday, February 05, 2010
New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
my comments to PLosone here ;
USA DEAD STOCK DOWNER COWS AND TME
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
PLEASE be aware, for 4 years, the USDA fed our children all across the Nation dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens. who will watch our children for CJD for the next 5+ decades ???
SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
----- Original Message -----
From: "Terry S. Singeltary Sr."
To: "Creutzfeldt-Jakob Disease"
Sent: Friday, May 21, 2010 2:27 PM
Subject: Re: [CJD-L] UPDATE - CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
Helane Shields also wrote the Government about this case (Thanks), only to recieve the same BSe i got ;
United States Department of Agriculture Food Safety and Inspection Service Washington. D.C. 20250 MAY 19, 2010
Dear Sir or Madam:
Thank you for your April 21, 2010, e-mail to the Department of Agriculture's (USDA) Food Safety and Inspection Service (FSIS) regarding allegations that a former slaughterhouse worker died from variant Creutzfeldt Jakob Disease (vCJD).
FSIS is the public health regulatory agency in USDA responsible for ensuring that meat, poultry, and processed egg products are safe, wholesome, and accurately labeled. FSIS enforces the Federal Meat Inspection Act, the Poultry Products Inspection Act, and the Egg Products Inspection Act, which require Federal inspection and regulation of meat, poultry, and processed egg products prepared for distribution in commerce for use as human food.
FSIS 'has not been informed that this death resulted from an occupational exposure. You may wish to contact the Centers for Disease Control and Prevention (CDC) at email@example.com. We share your concerns about vCJD-a rare, degenerative, fatal brain disorder in humans. Although not scientifically proven, there is strong epidemiologic and laboratory data linking vCJD to the consumption of beef contaminated with Bovine Spongiform Encephalopathy (BSE). For questions concerning vCJD, or any specific human disease, you may also wish to visit the CDC. Web site at http://www.cdc.gov. A fact sheet on vCJD is available at
http://www.cdc.gov/ncidod/dvrd/vcjd/factsheet_nvcjd.htm additional information at http://www.cdc.gov/ncidod/dvrd/vcjd.
You may also visit the World Health Organization (WHO) Web site at http://www.who.int/mediacentre/factsheets/fs180/en/. WHO is the directing and coordinating authority for health within the United Nations system. For more information on BSE, please visit the FSIS Web site at http://www.fsis.usda.gov/Fact_Sheets/Bovine_Spongiform_Encephalopathy_Mad_Cow_Disease/index.asp and http://www.fsis.usda.gov/Fact_Sheets/Bovine_Spongiform_Encephalopathy_BSE/index.asp.
Again, thank you for writing.
David P. Goldman, M.D., M.P.H. Assistant Administrator Office of Public Health Science
Wednesday, March 31, 2010
Atypical BSE in Cattle
Transmissible Spongiform Encephalopathy
Monday, April 5, 2010
Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010
----- Original Message ----- From: "Terry S. Singeltary Sr."
----- Original Message ----- From: Katie Glisic To: Terry S. Singeltary Sr. Sent: Monday, April 05, 2010 7:39 AM Subject: Re: [cjdsurv] CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
Dear Mr. Singelteary,
Thank you for contacting the Center. We are aware of Ms. Andablo's case and are in the process of testing, however thank you very much for the enclosed information. As you are aware, there have been no confirmed cases of vCJD (Mad Cow) contracting in the United States. The Center has been testing and diagnosing cases of CJD for over 10 years and reporting our findings to the Centers for Disease Control and Prevention. Of the two cases we have documented, neither was contracting in the US. One was contracted in the UK where cases of Mad Cow are known and one was contracted in Saudi Arabia.
Please note, we also performed the testing on Ms. Vinson and her family is well informed of the diagnosis provided by the Center. The United States government as well as the USDA go to great lengths to ensure that the US beef consumed by our country is both safe and continually tested to prevent outbreaks of food born illnesses such as Mad Cow. Please rest assured that Dr. Gambetti and the rest of the Center's researchers work tirelessly to provide accurate diagnosis to families with loved ones suffering from CJD.
On Fri, Apr 2, 2010 at 12:38 PM, Terry S. Singeltary Sr.
Greetings Professor Gambetti Sir,
A kind greetings from sunny Bacliff, Texas !
Sadly, i thought i should pass this data to you. You are probably much aware of this, but it seems odd that no media has commented? also, the last suspect nvCJD case i remember here in the USA, it was the USDA that the so called 'confidentiality agreements between family', and came out officially first and over ruled the nvCJD and called in sporadic CJD, well, i don't think they ever even officially called it that, but Aretha N. Vinson family knows what she had, and PD Notebook won in the end ;
Portsmouth woman did not die of mad cow-related condition, ___USDA___ says
By Nancy Young The Virginian-Pilot © May 7, 2008
(towards the end of this blog...tss)
Professor Gambetti Sir, Thank You for your continued work on TSE and all. ....
Kindest Regard and very Respectfully,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
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. <<<
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
Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence.She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers.
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.
>>> 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. <<<
Irma Linda Andablo, victima de CJD
"...padeció durante un año de CJD Esporádico, Falleció a la edad de 38 años en la ciudad de Mesquite Texas un 6 de Febrero del año 2010" Irma Linda Martinez nació en el pueblo de Batesville Texas un 17 de mayo de 1971, padeció durante un año de CJD Esporádico (mal de la vaca loca conocido en español) Falleció a la edad de 38 años en la ciudad de Mesquite Texas un 6 de Febrero del año 2010. A continuación describiremos datos de su padecimiento: Se casó a la edad de 16 años con Everardo Andablo (Lalo) ella residió en Lexington Nebraska, desde ese entonces, trabajó aproximadamente 11 años en una compañia de matanza de vacas y procesadora de carne (Tyson) ella trabajaba en el rastro o el área de matanza, para el 2008 ella trabajaba como agente de seguridad para esta misma compañia, para ese entonces ella empezó a presentar cambios en su vida, su próximo trabajo fue en Subway dentro de una tienda comercial, donde los cambios de salud empezaron a ser muy notorios pues empezó a perder mucho peso, de 237 L de su peso normal empezó perdiendo 24 L en menos de un mes, esto era sorprendente!!! fué entonces cuando dejó el trabajo en febrero del 2009, de repente empezó a olvidar datos importantes. La siguiente información es una traducción pertenece al comunicado que el equipo de neurologia del hospital Parkland en la ciudad de Dallas Texas liberó a su salida, después de haber estado internada del 29 de diciembre del 2009 a enero 20 del 2010, en este comunicado se encuentra el historial tanto médico como de sintomas presentados en Linda: Physician Discharge Summary : (traducido y adaptado) "...Mujer de 38 años presento 10 meses de una estado mental progresivo y alterado, con debilidad general, temblor, inhabilidad para caminar, para hablar, con pérdida de apetito e incontinencia de esfínteres, ella empezó a mostrar debilidad en las piernas, durante los siguientes meses su estado mental se agravó al tanto que ella no conoció más a sus propios hijos" "El 29 de Diciembre del 2009 Fué admitida en el Hospital Parkland de Dallas por demencia de acuerdo a los síntomas de presentaba, Mujer de 38 años presentó 14 meses de una estado mental progresivo y alterado, con debilidad general, temblor, inhabilidad para caminar, para hablar, con pérdida de apetito e incontinencia de esfinteres. Ella empezó a olvidar los nombres de las personas que la rodeaban, datos importantes personales, también presentó algunos cambios de personalidad como incremento de agresión.Para el mes de Marzo del 2008 ella empezó a mostrar debilidad en las piernas, durante los siguientes meses su estado mental se agravó al tanto que ella no conoció más a sus propios hijos (6 hijos), ella cada vez comia menos, cada vez perdia más peso.Para el tiempo que ella arrivo a Dallas para la navidad del 2009 ella no caminaba en lo absoluto, no hablaba solo hacia sonidos agresivos cuando alguien se acercaba a ella, el temblor en sus manos empezó a ser más fuerte, sus manos solo tenian posición de sostener algo fuerte, ella siempre.
"...padeció durante un año de CJD Esporádico, Falleció a la edad de 38 años en la ciudad de Mesquite Texas un 6 de Febrero del año 2010"
Irma Linda Martinez nació en el pueblo de Batesville Texas un 17 de mayo de 1971, padeció durante un año de CJD Esporádico (mal de la vaca loca conocido en español) Falleció a la edad de 38 años en la ciudad de Mesquite Texas un 6 de Febrero del año 2010.
A continuación describiremos datos de su padecimiento:
Se casó a la edad de 16 años con Everardo Andablo (Lalo) ella residió en Lexington Nebraska, desde ese entonces, trabajó aproximadamente 11 años en una compañia de matanza de vacas y procesadora de carne (Tyson) ella trabajaba en el rastro o el área de matanza, para el 2008 ella trabajaba como agente de seguridad para esta misma compañia, para ese entonces ella empezó a presentar cambios en su vida, su próximo trabajo fue en Subway dentro de una tienda comercial, donde los cambios de salud empezaron a ser muy notorios pues empezó a perder mucho peso, de 237 L de su peso normal empezó perdiendo 24 L en menos de un mes, esto era sorprendente!!! fué entonces cuando dejó el trabajo en febrero del 2009, de repente empezó a olvidar datos importantes.
La siguiente información es una traducción pertenece al comunicado que el equipo de neurologia del hospital Parkland en la ciudad de Dallas Texas liberó a su salida, después de haber estado internada del 29 de diciembre del 2009 a enero 20 del 2010, en este comunicado se encuentra el historial tanto médico como de sintomas presentados en Linda:
Physician Discharge Summary : (traducido y adaptado)
"...Mujer de 38 años presento 10 meses de una estado mental progresivo y alterado, con debilidad general, temblor, inhabilidad para caminar, para hablar, con pérdida de apetito e incontinencia de esfínteres, ella empezó a mostrar debilidad en las piernas, durante los siguientes meses su estado mental se agravó al tanto que ella no conoció más a sus propios hijos"
"El 29 de Diciembre del 2009 Fué admitida en el Hospital Parkland de Dallas por demencia de acuerdo a los síntomas de presentaba, Mujer de 38 años presentó 14 meses de una estado mental progresivo y alterado, con debilidad general, temblor, inhabilidad para caminar, para hablar, con pérdida de apetito e incontinencia de esfinteres. Ella empezó a olvidar los nombres de las personas que la rodeaban, datos importantes personales, también presentó algunos cambios de personalidad como incremento de agresión.Para el mes de Marzo del 2008 ella empezó a mostrar debilidad en las piernas, durante los siguientes meses su estado mental se agravó al tanto que ella no conoció más a sus propios hijos (6 hijos), ella cada vez comia menos, cada vez perdia más peso.Para el tiempo que ella arrivo a Dallas para la navidad del 2009 ella no caminaba en lo absoluto, no hablaba solo hacia sonidos agresivos cuando alguien se acercaba a ella, el temblor en sus manos empezó a ser más fuerte, sus manos solo tenian posición de sostener algo fuerte, ella siempre portaba pelotas pequeñas para que no se lastimara con sus propias uñas"
En terminos Médicos ella prensento un desorden mental con ansiedad y pérdida del habla y contracciones en los musculos que la inmobilizaba. Esto llevo a los médicos a predecir el diagnostico de CJD esporádico o variante, después de reuniones familiares se llego al acuerdo de no proseguir con los exámenes indicados como una biopsia cerebral debido al estado de debilidad y gravedad de ella, pues peligraba su vida y por consiguiente peligraban los médicos que le aplicarian el exámen ya que es demasiado contagioso.
Ella fué dada de alta con el diagnostico de CJD Esporádico, sin medicamento y con pocas esperanzas y semanas de vida.
please see full text ;
Monday, March 29, 2010
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
YOU can be assured they are squirming behind closed doors, and that they are doing there best to squirm right out of this one. they will come up with something, international travel long ago, or some strange PRNP mutation that they might say like sporadic ffi ??? or a case of atypical case of inherited Creutzfeldt-Jakob disease (CJD) ??? they will make up something. but it will be anything but BSE related here in the USA, in my opinion. sporadic FFI, or sporadic GSS, or sporadic inherited CJD is an oxymoron. it's either familial or not. or even this new novel human disease known as Protease-Sensitive Prionopathy (PSPr), they might come up with that. if they cannot do this, it will be an occupational TSE infection, whether they want to admit it or not. and they don't admit those to often, they cover them up. just like that Spanish Doctor that handled cjd infected tissue. but we never heard nothing about that one either ;
Investigator succumbs to CJD THE head of Pathological Anatomy at Principe de Asturias hospital in Alcala de Henares, Dr Antonio Ruiz Villaescusa, has died from Creutzfeldt-Jakob's disease. It is believed that Dr Ruiz, a specialist in CJD, contracted the disease after exposure to tissue from infected patients.
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.
please see full text ;
Wednesday, March 31, 2010
Atypical BSE in Cattle
Sunday, March 28, 2010
Nor-98 atypical Scrapie, atypical BSE, spontaneous TSE, trade policy, sound science ?
*****URGENT NOTE HERE ABOUT OIE AND THEIR JUNK SCIENCE ABOUT ATYPICAL BSE*****
Wednesday, March 31, 2010
Atypical BSE in Cattle
CJD SURVEILLANCE TEXAS
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Monday, April 5, 2010
UPDATE - CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER