USA cases of dpCJD rising with 24 cases so far in 2010
Greetings,
please be aware, i have termed this strange strain of 'diagnosis pending creutzfeldt jakob disease' as 'dpCJD', what ever that is suppose to mean. how many more years, decades, are we going to have to flounder for them to establish another name for the same disease ?
5 Includes 28 cases in which the diagnosis is pending, and 17 inconclusive cases;
6 Includes 28 (24 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded
http://www.cjdsurveillance.com/pdf/case-table.pdf
Let's review some history ;
IDIOPATHIC BRAIN STEM NEURONAL CHROMATOLYSIS AND HIPPOCAMPAL SCLEROSIS
(VET REC 1992, M Jeffrey, J W Wilesmith p359-362)
snip...
BRIEFING
1. The disease title is comlex and invites the press to coin a new one (such as BSE II, MAD COW II, or Son of BSE). It is suggested for now that it is called a brain disorder or brain dgeneration (BD).
BD - THE LINE TO TAKE
2. Disease clinically similar to BSE but pathologically distinct. BD is NOT a form of BSE.
snip...
R BRADLEY
20 October 1992
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1992/10/20003001.pdf
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1992/10/20003001.pdf
Martin Jeffrey observes that there is a strong similarity between the histopathological picture in BBD and that produced by ME7 strain of Scrapie in mice.
snip...
7. There have to date been 42 cases of BBD out of a total of 2,598 brains submitted for BSE diagnosis in Scotland. The incidence of the condition appears to be 1 in 10,000 of beef suckler cows.
W L GARDNER VHS
23 October 1992
92/10.23/2.2
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1992/10/23002001.pdf
''THE LINE TO TAKE'' ON IBNC $$$ 1995 $$$
1995
page 9 of 14 ;30. The Committee noted that the results were unusual. the questioned whether there could be coincidental BSE infection or contamination with scrapie. Dr. Tyrell noted that the feeling of the committee was that this did not represent a new agent but it was important to be prepared to say something publicly about these findings. A suggested line to take was that these were scientifically unpublishable results but in line with the policy of openness they would be made publicly available and further work done to test their validity. Since the BSE precautions were applied to IBNC cases, human health was protected. Further investigations should be carried out on isolations from brains of IBNC cases with removal of the brain and subsequent handling under strict conditions to avoid the risk of any contamination.31. Mr. Bradley informed the Committee that the CVO had informed the CMO about the IBNC results and the transmission from retina and he, like the Committee was satisfied that the controls already in place or proposed were adequate. ...
snip... see full text
http://collections.europarchive.org/tna/20090114154722/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
this information had been proved to be incorrect for a number of reasons...
http://web.archive.org/web/20030327015011/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS
"All of the 15 cattle tested showed that the brains had abnormally accumulated PrP"
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
Wednesday, October 08, 2008
Idiopathic Brainstem Neuronal Chromatolysis (IBNC): a novel prion protein related disorder of cattle?
http://bse-atypical.blogspot.com/2008/10/idiopathic-brainstem-neuronal.html
''LINE TO TAKE"
6. Trouble has been brewing for some time. Dr Collinge is lobbying hard, and threatening to go to the media, claiming Dr Will is blocking his research...
snip...
9. ...There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimers and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest. ...
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Thursday, November 05, 2009
Incidence and spectrum of sporadic Creutzfeldt-Jakob disease variants with mixed phenotype and co-occurrence of PrPSc types: an updated classification
http://creutzfeldt-jakob-disease.blogspot.com/2009/11/incidence-and-spectrum-of-sporadic.html
Thursday, July 10, 2008
A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.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
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
Monday, April 5, 2010
UPDATE - CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
http://prionunitusaupdate2008.blogspot.com/2010/04/update-cjd-texas-38-year-old-female.html
Monday, March 29, 2010
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas
http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo-cjd-victim-she-died.html
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
Thursday, May 27, 2010
CDC - INQUIRY ABOUT vCJD DEATH OF SLAUGHTER HOUSE WORKER IRMA LINDA ANDABLO
http://cjdtexas.blogspot.com/2010/05/cdc-inquiry-about-vcjd-death-of.html
Archive Number 20100405.1091 Published Date 05-APR-2010
Subject PRO/AH/EDR> Prion disease update 1010 (04)
snip...
[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.
http://whqlibdoc.who.int/publications/2003/9241545887.pdf
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?"
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
Questions linger in U.S. CJD cases
Published: Oct. 21, 2005 at 9:49 PM
By STEVE MITCHELL, Senior Medical Correspondent
WASHINGTON, Oct. 21 (UPI) -- French researchers have ruled out the human form of mad cow disease in a deceased California man, even though they did not conduct the critical test widely regarded as the only way to determine precisely the nature of his disease, United Press International has learned.
The case of Patrick Hicks, who died last November from his condition, has remained murky from the beginning. Dr. Ron Bailey, of Riverside, Calif., the man's neurologist, had suspected the 49-year-old Hicks of having contracted variant Creutzfeldt Jakob disease -- a fatal, brain-wasting illness humans can contract from eating beef products contaminated with the mad cow pathogen -- and both he and the family wanted an autopsy conducted to determine if Hicks had succumbed to the disorder.
Bailey became concerned that Hicks might have contracted vCJD because he initially had exhibited psychiatric symptoms, his illness appears to have lasted for more than one year and he showed normal brain-wave patterns via EEGs until the late stages -- all consistent with the disease. In addition, Hicks's relatively young age raised concerns, because nearly all of the more than 150 cases of vCJD detected worldwide have occurred in people under age 55.
The first hint of oddness began when, according to both Hicks's brother and mother, a team of six doctors, who they suspect were with the Centers for Disease Control and Prevention in Atlanta, visited Patrick last October while he was still alive and under care at Loma Linda University Medical Center in Loma Linda, Calif.
They said they were asked to leave when the doctors arrived to examine Patrick.
CDC officials would not confirm to UPI whether they had investigated the case, but the agency's policy does require examining all suspected cases of vCJD in anyone under 55.
The family also said Loma Linda refused to released Hicks's medical records to them.
The oddities continued after Hicks's death. Bailey found it almost impossible to get an autopsy conducted on Hicks, the only way to determine conclusively whether he had variant or sporadic CJD -- a version of the disease not related to mad cow. One county coroner's office referred him to another and both refused to conduct the procedure, he said.
Then, the National Prion Disease Pathology Surveillance Center in Cleveland, Ohio -- which was established by the CDC to investigate potential vCJD cases in the United States -- dispatched a mobile autopsy company called 1-800-Autopsy, but the company failed to follow the center's protocol and did not collect frozen sections of brain, which are required for tests to determine whether the disease is vCJD or sCJD. Instead, the autopsy company fixed the entire brain in formalin.
The NPDPSC, however, considers the collection of frozen brain tissue essential to distinguishing vCJD from other forms of CJD.
"Only frozen brain tissue examination definitely confirms or excludes the diagnosis of prion disease and provides the information to identify the type of prion disease," the center's Web site says. Prions are abnormal proteins thought to play a role in causing vCJD and sCJD.
The problem raised enough concern that both Bailey and Hicks's family sought a second opinion.
Experts had told them that animal-injection studies could be done with formalin-fixed tissue, so the family arranged to have a sample of Patrick's brain sent to Dr. Jean Jacques Hauw at the Laboratoire De Neuropathologie at the Groupe Hospitalier Pitie-Salpetriere in Paris, who they thought had agreed to do the studies.
The NPDPSC, however, delayed sending the sample to France for two months after the family's request last March. During the delay, Pierluigi Gambetti, the NPDPSC's director, sent a letter to Hicks's wife.
"We can definitely rule out the diagnosis of variant CJD," the letter stated.
Gambetti's strong conclusion sounded strange to Bailey, because the NPDPSC had not conducted further tests since January, when they had said vCJD was unlikely but that they were unable to rule it out entirely.
After examining the brain tissue, Hauw's team told the family the disease was consistent with sCJD, but to date they have not explained why they did not conduct the animal-injection studies -- the family's reason for sending samples of his brain to France.
Asked the reasons for not following the family's wishes and conducting the animal studies, Hauw told UPI, "I cannot answer your question," citing French regulations that prohibited him from providing information about a specific patient.
He did say, however, that "animal injection is not needed for the routine diagnosis of Creutzfeldt-Jakob disease and its various variants, at least in France and in the United Kingdom."
That may be true, but it remains unclear why he accepted the case in the first place, knowing that is what the family wanted.
Moreover, this was not a "routine diagnosis." If Hicks suffered from vCJD, he potentially would have been the first person in the United States to have acquired the disease domestically, a development with significant domestic and international ramifications.
In addition, other experts, such as Dr. Laura Manuelidis, section chief of surgery in the neuropathology department at Yale University, have said the only way to know conclusively whether the disease is due to sCJD or vCJD is through animal-injection studies.
"From what I gather, the result was merely rubber stamped," Bailey told UPI. "I guess we will never really know for sure."
The handling of the case is noteworthy, because the NPDPSC currently is investigating nine potential sCJD cases in Idaho. Experts suspect some of those cases could be vCJD.
Bailey and some patient advocates said they are now skeptical of the NPDPSC's behavior.
"How could my experience with the Hicks case ... and the interaction with NPDPSC not lessen my confidence?" Bailey asked. "I anticipate that all of the Idaho cluster of CJD patients will turn out to have sCJD. I cannot for a minute see their results indicating anything but this. After all, if any patient were to have vCJD, it would have been Patrick Hicks. The results of NPDPSC are not definitive in excluding Hicks as not having vCJD. There certainly will always be that question in my mind."
Terry Singletary, a patient advocate whose mother died of a form of the disease called Heidenhain variant, told UPI he likewise had lost confidence in the NPDPSC.
"I do not trust them," Singletary said. "It's all going to be sporadic. This is the way they want it. They do not want to find out all the routes and sources of this agent."
Both vCJD and mad cow disease are politically sensitive issues because they can impact international trade. Dozens of nations closed their borders to American beef after a lone U.S. cow tested positive for the disease in 2003, resulting in more than $4.7 billion in losses for the industry, and the U.S. Department of Agriculture delayed doing confirmatory tests for seven months on what turned out to be a second case of mad cow.
The NPDPSC did not respond to UPI's phone call requesting comment about the Idaho cases. The CDC referred UPI to Idaho officials.
Of the nine Idaho cases, three people have tested positive for a CJD-like illness, but officials are conducting further tests to determine whether the disease is sCJD. Two others tested negative and four were buried without autopsies.
The cases could just be a statistical fluke, but the state averages about 1.2 sCJD cases per year and has never had more than three in a single year. The disease is rare and generally is thought to occur at the rate of one case per million people.
Several CJD clusters in other states have far exceeded that rate, however. These included:
--southern New Jersey (2000-2003),
--Lehigh, Pa. (1986-90),
--Allentown, Pa. (1989-92),
--Tampa, Fla. (1996-97),
--Oregon (2001-02), and
--Nassau County, N.Y. (1999-2000).
Some of the clusters involved as many as 18 deaths, and ranged from a rate of four to eight cases per million people.
A group of J.P. Morgan analysts issued an advisory last year on the impact the clusters could have on the beef industry, and said that some of the cases could be due to vCJD.
"The existence of clusters raises the question of 'contamination' or 'infection,' and also raises the hypothesis that rather than cases of sCJD, these might have been cases of vCJD," the advisory said. "Given that sCJD occurs randomly in one out of 1 million cases, it is a statistical rarity to find an sCJD cluster -- let alone six."
If that assessment is accurate, another cluster in Idaho would be even more unlikely.
Another possibility is some of the Idaho cases could be due to chronic wasting disease, which is similar to mad cow disease and currently is epidemic among deer and elk in several states, including Idaho's neighbors Wyoming and Utah.
No human cases of CWD have ever been confirmed, but the disease has been shown to infect human cells in a lab dish. Also, a team of researchers led by Jason Bartz of Creighton University in Omaha, Neb., report in the November issue of the Journal of Virology they had experimentally transmitted CWD to squirrel monkeys --the first reported transmission of CWD to primates.
If CWD is capable of infecting humans, it is unknown whether the resulting disease would resemble sCJD, vCJD or a novel disorder. If the disease looks like sCJD, cases could be going undetected or misdiagnosed.
--
E-mail: healthbiz@upi.com
http://www.upi.com/Health_News/2005/10/21/Questions-linger-in-US-CJD-cases/UPI-65761129945790/
NIH may destroy human brain collection
By Steve Mitchell Medical Correspondent
Washington, DC, Mar. 24 (UPI) -- The National Institutes of Health may discard part or all of a rare collection that includes hundreds of human brain samples from patients that suffered from a disorder similar to mad cow disease -- unless another researcher or institution takes them on, United Press International has learned.
see full history of the day they almost destroyed all donated brains samples from CJD victims ;
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html
3.56 A further difference in the transmission properties of the two diseases was the pattern of disease caused in the brains of experimental animals. Mice inoculated with scrapie material from geographically and temporally distinct sources were found to have variable brain lesions, whereas mice inoculated with BSE material similarly derived from different sources all had very similar patterns of disease. 30 These results showed that, unlike scrapie, only one strain of BSE was present in the inocula derived from different sources. As the current hypothesis suggested that scrapie had transmitted to cattle at a number of geographically separate sites, it might have been expected that several strains of BSE would have been evident, given that over 20 strains of scrapie were known. Since 1996, strain-typing studies in mice have shown that the lesion profile produced by BSE is different to all known scrapie strains. 31
3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.
3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988, 35 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988-89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA. 36 It was also felt that the results of such an experiment would be hard to interpret. While a negative result would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE. 37 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest. 38
3.59 Nevertheless, from the first demonstration of transmissibility of BSE in 1988, the possibility of differences in the transmission properties of BSE and scrapie was clear. Scrapie was transmissible to hamsters, but by 1988 attempts to transmit BSE to hamsters had failed. Subsequent findings increased that possibility.
http://web.archive.org/web/20010224062436/http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820550
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html
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
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Friday, February 05, 2010
New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review
http://vcjd.blogspot.com/2010/02/new-variant-creutzfelt-jakob-disease.html
Thursday, May 06, 2010
Sporadic Creutzfeldt-Jakob disease mimicking nonconvulsive status epilepticus
http://creutzfeldt-jakob-disease.blogspot.com/2010/05/sporadic-creutzfeldt-jakob-disease.html
Sunday, February 14, 2010
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html
Wednesday, February 24, 2010
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th
ICID International Scientific Exchange Brochure -
http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html
TSE
http://transmissiblespongiformencephalopathy.blogspot.com/
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
Showing posts with label CJD. Show all posts
Showing posts with label CJD. Show all posts
Tuesday, June 1, 2010
Monday, March 29, 2010
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
URGENT, PLEASE NOTE ;
>>> 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.
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.
http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8
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... Read more...
http://www.recordandoalinda.com/
"...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.
http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=2:frontpage&catid=1:frontpage
>>> 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. <<<
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.
http://www.euroweeklynews.com/news_spanish_press.html
http://74.125.47.132/search?q=cache:MfWnPKrMDEwJ:www.euroweeklynews.com/news_spanish_press.html+Principe+de+Asturias+in+Alcala+de+Henares+cjd&cd=5&hl=en&ct=clnk&gl=us
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html
TSS
Wednesday, February 24, 2010
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th ICID International Scientific Exchange Brochure -
http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html
TSE
http://transmissiblespongiformencephalopathy.blogspot.com/
Sunday, March 28, 2010
Nor-98 atypical Scrapie, atypical BSE, spontaneous TSE, trade policy, sound science ?
http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html
DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)
The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why????than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!! Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....
Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!
And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...
Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"
again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.
You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)
snip...end
CJD SURVEILLANCE TEXAS
http://cjdtexas.blogspot.com/2007/12/creutzfeldt-jakob-disease-surveillance.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
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.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007
(occupational exposure to prion diseases)
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html
Tuesday, March 16, 2010
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 REVISED FEB. 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/03/transmissible-spongiform-encephalopathy.html
Monday, March 29, 2010
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas
http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo-cjd-victim-she-died.html
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
>>> 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.
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.
http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8
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... Read more...
http://www.recordandoalinda.com/
"...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.
http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=2:frontpage&catid=1:frontpage
>>> 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. <<<
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.
http://www.euroweeklynews.com/news_spanish_press.html
http://74.125.47.132/search?q=cache:MfWnPKrMDEwJ:www.euroweeklynews.com/news_spanish_press.html+Principe+de+Asturias+in+Alcala+de+Henares+cjd&cd=5&hl=en&ct=clnk&gl=us
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html
TSS
Wednesday, February 24, 2010
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th ICID International Scientific Exchange Brochure -
http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html
TSE
http://transmissiblespongiformencephalopathy.blogspot.com/
Sunday, March 28, 2010
Nor-98 atypical Scrapie, atypical BSE, spontaneous TSE, trade policy, sound science ?
http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html
DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)
The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why????than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!! Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....
Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!
And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...
Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"
again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.
You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)
snip...end
CJD SURVEILLANCE TEXAS
http://cjdtexas.blogspot.com/2007/12/creutzfeldt-jakob-disease-surveillance.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
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.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007
(occupational exposure to prion diseases)
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html
Tuesday, March 16, 2010
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 REVISED FEB. 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/03/transmissible-spongiform-encephalopathy.html
Monday, March 29, 2010
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas
http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo-cjd-victim-she-died.html
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
Friday, October 23, 2009
Creutzfeldt-Jakob Disease Surveillance Texas Data for Reporting Years 2000-2008
Creutzfeldt-Jakob Disease Surveillance Data for Reporting Years 2000-2008
A total of 119 people died from CJD during 2000-2008. Texas has had one variant CJD case. Investigators have concluded that the patient was a former resident of the UK where exposure was likely to have occurred.
CJD cases* in Texas by gender and age 2000–2008†
Characteristics 2000 2001 2002 2003 2004 2005 2006 2007 2008 Total
Gender Male 10 8 3 6 10 7 7 5 8 64
Female 4 6 4 10 3 8 2 9 8 54
Age (years)
< 55 3 0 3 4 3 4 3 3 3 26
≥ 55 11 14 4 12 10 11 6 11 13 92
* based on data as of March 30, 2009
† Includes cases of possible, probable and confirmed sporadic CJD and confirmed familial CJD
http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/data/
Reporting Creutzfeldt-Jakob Disease
Several Texas laws (Tex. Health & Safety Code, Chapters 81, 84 and 87) require specific information regarding notifiable conditions be provided to the Texas Department of State Health Services (DSHS). Health care providers, hospitals, laboratories, schools, and others are required to report patients who are suspected of having a notifiable condition (25 Tex. Admin. Code §97.2 ).
Report Creutzfeldt-Jakob Disease (CJD) within one week. Reporting Forms >>
http://www.dshs.state.tx.us/idcu/investigation/forms/CJD.pdf
CJD became a notifiable condition in 1998 in Texas. Suspected cases of CJD should be reported to local health departments by dialing 1-800-705-8868.
In September 1997, the National Prion Disease Pathology Surveillance Center (NPDPSC) was established at the Division of Neuropathology of Case Western Reserve University to, among other functions, assist clinicians in the diagnosis of prion disease. The NPDPSC assists clinicians by analyzing cerebrospinal fluid, blood, and brain tissue. Information about diagnostic services, protocols for various CJD testing, and specimen submission can be obtained at
http://www.cjdsurveillance.com
or by contacting the director, Dr. Pierluigi Gambetti or staff at the Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Room 419, Cleveland, Ohio 44106; Phone, 216/368-0587; Fax, 216/368-4090; E-mail, cjdsurv@po.cwru.edu .
Physicians are strongly encouraged to confirm the diagnosis of CJD by arranging for an autopsy following the death of the person suspected of having CJD. This is especially important if the person had an onset at age less than 55. Please contact the center above for assistance or specimen submission.
http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/reporting/
Have There Been Any Cases of “Mad Cow Disease” in the United States? Bovine spongiform encephalopathy (BSE) or “mad cow disease” is a disease specific to cattle. There have been three cases of BSE in cattle identified in the United States. The first case of BSE was identified in Washington State (2002) and the cow was found to have been imported from Canada. In 2004 BSE was identified in a Texas-born cow representing the first native case in the United States. A second native case was reported in an Alabama bovine in 2006.
Have There Been Any Cases of Variant CJD in the United States? Yes, there have been three cases of variant CJD identified in humans in the United States. The first case-patient was born in the United Kingdom in the late 1970s and lived there until relocating to Florida in 1995. Onset of symptoms began in 2001 and the patient died in 2004. The second case–patient was born and raised in England before moving to Texas in 2001. Symptoms began in 2005 and were confirmed neuropathologically (by autopsy) in 2006 by experts in the United Kingdom. Both the first and second case-patients are believed to have been exposed to the BSE agent while residing in the United Kingdom during the defined period of risk (1980–1996). The third case–patient was born and raised in Saudi Arabia and resided in the United States since 2005. Variant CJD was neuropathologically confirmed by biopsy in 2006. Investigators believe that exposure most likely occurred from consumption of contaminated cattle while residing in Saudi Arabia as a child.
http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/faqs/
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
Creutzfeldt-Jakob Disease in Northeast Texas,
J.A. Rawlings,*1 K.A. Hendricks1, O.M. Nuno1, D.A. Brown1, D.A. Evans2, Texas Department of Health, 1Austin and 2Tyler, Texas
Creutzfeldt-Jacob Disease (CJD), a transmissible spongiform encephalopathy, is caused by prions composed of proteinaceous material devoid of nucleic acid. CJD occurs sporadically (generally 1 case/1,000,000 population per year) in older patients (average age of 65) and is characterized by rapidly progressive dementia, accompanied by severe muscle spasms and incoordination. Death usually occurs within 3 to 12 months (average 7 months). CJD activity in Texas, which has a population of nearly 19 million, appeared to be typical. The statewide death rate for 1995 and 1996 was just under 1/1,000,000. In April of 1997, the Texas Department of Health became aware of an increased number of possible CJD cases in a 23-county area of NE Texas with a population of just over one million. After review of medical and pathology records, four patients were identified with definite classic CJD and three were identified with probable CJD. Dates of death for the eight patients were from April, 1996 through mid-July 1997. The patients were from 46 through 65 years of age; four were male and three were female. A case-control study to identify risks for CJD in NE Texas has been initiated.
http://www.jifsan.umd.edu/tse/Rawlings.htm
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Sunday, December 16, 2007
Creutzfeldt-Jakob Disease Surveillance in Texas 2000-2006
http://cjdtexas.blogspot.com/2007/12/creutzfeldt-jakob-disease-surveillance.html
Creutzfeldt-Jakob Disease Surveillance in Texas
http://cjdtexas.blogspot.com/
Tuesday, August 11, 2009
Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html
TSS
A total of 119 people died from CJD during 2000-2008. Texas has had one variant CJD case. Investigators have concluded that the patient was a former resident of the UK where exposure was likely to have occurred.
CJD cases* in Texas by gender and age 2000–2008†
Characteristics 2000 2001 2002 2003 2004 2005 2006 2007 2008 Total
Gender Male 10 8 3 6 10 7 7 5 8 64
Female 4 6 4 10 3 8 2 9 8 54
Age (years)
< 55 3 0 3 4 3 4 3 3 3 26
≥ 55 11 14 4 12 10 11 6 11 13 92
* based on data as of March 30, 2009
† Includes cases of possible, probable and confirmed sporadic CJD and confirmed familial CJD
http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/data/
Reporting Creutzfeldt-Jakob Disease
Several Texas laws (Tex. Health & Safety Code, Chapters 81, 84 and 87) require specific information regarding notifiable conditions be provided to the Texas Department of State Health Services (DSHS). Health care providers, hospitals, laboratories, schools, and others are required to report patients who are suspected of having a notifiable condition (25 Tex. Admin. Code §97.2 ).
Report Creutzfeldt-Jakob Disease (CJD) within one week. Reporting Forms >>
http://www.dshs.state.tx.us/idcu/investigation/forms/CJD.pdf
CJD became a notifiable condition in 1998 in Texas. Suspected cases of CJD should be reported to local health departments by dialing 1-800-705-8868.
In September 1997, the National Prion Disease Pathology Surveillance Center (NPDPSC) was established at the Division of Neuropathology of Case Western Reserve University to, among other functions, assist clinicians in the diagnosis of prion disease. The NPDPSC assists clinicians by analyzing cerebrospinal fluid, blood, and brain tissue. Information about diagnostic services, protocols for various CJD testing, and specimen submission can be obtained at
http://www.cjdsurveillance.com
or by contacting the director, Dr. Pierluigi Gambetti or staff at the Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Room 419, Cleveland, Ohio 44106; Phone, 216/368-0587; Fax, 216/368-4090; E-mail, cjdsurv@po.cwru.edu .
Physicians are strongly encouraged to confirm the diagnosis of CJD by arranging for an autopsy following the death of the person suspected of having CJD. This is especially important if the person had an onset at age less than 55. Please contact the center above for assistance or specimen submission.
http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/reporting/
Have There Been Any Cases of “Mad Cow Disease” in the United States? Bovine spongiform encephalopathy (BSE) or “mad cow disease” is a disease specific to cattle. There have been three cases of BSE in cattle identified in the United States. The first case of BSE was identified in Washington State (2002) and the cow was found to have been imported from Canada. In 2004 BSE was identified in a Texas-born cow representing the first native case in the United States. A second native case was reported in an Alabama bovine in 2006.
Have There Been Any Cases of Variant CJD in the United States? Yes, there have been three cases of variant CJD identified in humans in the United States. The first case-patient was born in the United Kingdom in the late 1970s and lived there until relocating to Florida in 1995. Onset of symptoms began in 2001 and the patient died in 2004. The second case–patient was born and raised in England before moving to Texas in 2001. Symptoms began in 2005 and were confirmed neuropathologically (by autopsy) in 2006 by experts in the United Kingdom. Both the first and second case-patients are believed to have been exposed to the BSE agent while residing in the United Kingdom during the defined period of risk (1980–1996). The third case–patient was born and raised in Saudi Arabia and resided in the United States since 2005. Variant CJD was neuropathologically confirmed by biopsy in 2006. Investigators believe that exposure most likely occurred from consumption of contaminated cattle while residing in Saudi Arabia as a child.
http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/faqs/
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
Creutzfeldt-Jakob Disease in Northeast Texas,
J.A. Rawlings,*1 K.A. Hendricks1, O.M. Nuno1, D.A. Brown1, D.A. Evans2, Texas Department of Health, 1Austin and 2Tyler, Texas
Creutzfeldt-Jacob Disease (CJD), a transmissible spongiform encephalopathy, is caused by prions composed of proteinaceous material devoid of nucleic acid. CJD occurs sporadically (generally 1 case/1,000,000 population per year) in older patients (average age of 65) and is characterized by rapidly progressive dementia, accompanied by severe muscle spasms and incoordination. Death usually occurs within 3 to 12 months (average 7 months). CJD activity in Texas, which has a population of nearly 19 million, appeared to be typical. The statewide death rate for 1995 and 1996 was just under 1/1,000,000. In April of 1997, the Texas Department of Health became aware of an increased number of possible CJD cases in a 23-county area of NE Texas with a population of just over one million. After review of medical and pathology records, four patients were identified with definite classic CJD and three were identified with probable CJD. Dates of death for the eight patients were from April, 1996 through mid-July 1997. The patients were from 46 through 65 years of age; four were male and three were female. A case-control study to identify risks for CJD in NE Texas has been initiated.
http://www.jifsan.umd.edu/tse/Rawlings.htm
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Sunday, December 16, 2007
Creutzfeldt-Jakob Disease Surveillance in Texas 2000-2006
http://cjdtexas.blogspot.com/2007/12/creutzfeldt-jakob-disease-surveillance.html
Creutzfeldt-Jakob Disease Surveillance in Texas
http://cjdtexas.blogspot.com/
Tuesday, August 11, 2009
Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html
TSS
Sunday, December 16, 2007
Creutzfeldt-Jakob Disease Surveillance in Texas 2000-2006
Sunday, December 16, 2007
Creutzfeldt-Jakob Disease Surveillance in Texas 2000–2006
Abstract
Creutzfeldt-Jakob disease (CJD) is a rare neurodegenerative disease caused by prions. The disease is usually fatal within a year and there is currently no known treatment or cure. CJD has been a reportable condition in Texas since 1998. There are currently four known types: sporadic, familial, variant, and iatrogenic. Diagnosis is complex and direct examination of brain tissue is required for case confirmation and identification of the type of CJD. During 2000–2006, there were 181 cases of confirmed, probable, or possible CJD diagnosed among Texas residents, including 88 cases of sporadic CJD, 5 cases of familial CJD, and 1 case of variant CJD. Most case-patients were male (55%) and 55 years of age or older (78%). The Texas Department of State Health Services is available to assist health care professionals with arrangement of free diagnostic testing and to provide resources for family support.
snip...
Texas Surveillance
CJD has been a reportable condition in Texas since 1998. The majority of CJD cases are reported to the Texas Department of State Health Services (DSHS) by test or autopsy reports received from the Prion Center. A few cases are discovered by routine death certificate review and some cases are reported by a local or regional health department, health care provider, or family member. Copies of results from all CJD-related testing performed by the Prion Center are sent to DSHS as a part of routine surveillance procedures. DSHS reviews test results and investigates all cases with positive test results including those with elevated CSF 14-3-3 protein levels. Table 1 summarizes the number of cases for all types of CJD in Texas (2000–2006). Each year in Texas, the total number of confirmed, probable, or possible sporadic CJD cases has remained somewhat constant (mean=13; range= 6–15). In addition, on average, one case of familial CJD was diagnosed each year in Texas during 2000–2006, all from separate families. Only 1 case of variant CJD has ever been diagnosed in Texas. The patient was a former resident of the United Kingdom, where the exposure was likely to have occurred. Texas has a population of 23 million, and since the national rate of sporadic CJD is about 1 per million, it is expected that approximately 23 cases of CJD would occur each year in the state. Therefore, it is believed that CJD is currently underreported in Texas. Table 2 describes sporadic and familial CJD cases in Texas according to gender and age. Of the patients diagnosed with CJD during 2000–2006, 58% were male and 79% were 55 years of age or older. Figure 1 depicts the number of CJD cases per county for the years 2000–2006. Note that higher numbers of cases are located in counties with higher populations.
CJD should be suspected and reported to DSHS in individuals who meet the following criteria:
1) Dementia of early onset (younger than 55 years of age) or 2) Rapidly progressive dementia and one of more of the following: • Movement disorder • Painful sensory symptoms • Visual disturbances or 3) Diagnosed by a physician as having CJD
Case Classification
The World Health Organization (WHO) established recommended standards for all types of CJD surveillance in 1997 (Table 3). The United States, including Texas, has adopted these surveillance standards to determine case classification for sCJD, fCJD and iCJD. For vCJD, CDC has developed diagnostic case criteria for use in the United States (Table 3). Direct examination of brain tissue through either biopsy or autopsy is highly recommended for all types of CJD and is required for confirmation of sporadic CJD and variant CJD. A sCJD case is determined to be ‘probable’ if there is enough diagnostic testing to suggest CJD but no autopsy has been performed. Patients considered for
probable sCJD must exhibit progressive dementia and have a typical EEG and/or elevated CSF 14-3-3 protein. In addition they must display at least 2 of 4 clinical features: myoclonus, visual or cerebellar disturbance, akinetic mutism, and/or pyramidal/extrapyramidal dysfunction. For a case to be listed as ‘possible’, the patient must have progressive dementia and at least 2 of the listed clinical features, disease duration of less than 2 years and either no EEG testing or EEG atypical for CJD. Iatrogenic CJD must have a known risk factor, e.g., high risk surgery or cadaver-derived pituitary hormone. Familial CJD is considered confirmed in a patient with a neuropsychiatric disorder if a first degree relative had confirmed or probable CJD or a disease-specific prion protein gene mutation has been identified. Table 3 describes the case classification for each type of CJD.
Conclusions
CJD is an emerging disease that may be misdiagnosed and appears to be underreported in Texas. As with other emerging diseases, the partnership of the medical community and public health epidemiologists provides a framework to share information and expertise among local, state, federal and international colleagues and to detect and respond to
diseases that are rapidly fatal, difficult to diagnose, and rare. Enhanced surveillance will provide a better understanding of the epidemiology of this disease and its impact and opportunities for mitigation. Recognition of possible CJD and reporting by health professionals is an integral part of CJD surveillance in Texas. CJD is a reportable disease in Texas. All suspected cases should be reported within one week to the Texas Department of State Health Services, Infectious Disease Control Unit. Confirmation and typing of the disease requires neuropathological confirmation by direct examination of brain tissue, usually postmortem, by the Prion Center. It is important to establish the precise type of CJD to help monitor disease occurrence especially for variant CJD. Physicians should strongly consider arranging for autopsies of suspected or clinically-diagnosed CJD patients. The Texas Department of State Health Services can assist health professionals by arranging free diagnostic testing and providing resources for family support.
References...snip...end...TSS
Table 1. Cases of Creutzfeldt-Jakob disease in Texas*§
Type 2000 2001 2002 2003 2004 2005 2006 Total
Sporadic
Confirmed 9 8 4 6 7 8 5 47
Probable 2 4 1 5 5 6 3 26
Possible 3 1 1 4 1 0 0 10
Subtotal 14 13 6 15 13 14 8 83
Familial 0 1 1 1 0 1 1 5
Iatrogenic 0 0 0 0 0 0 0 0
Variant 0 0 0 0 0 0 1† 1
Total 14 14 7 16 13 15 10 89
*Based on data as of June 15, 2007.
† Confirmed in United Kingdom and reported to Texas Department of State Health Services through Centers for Disease Control and Prevention.
§ Based on year of death.
Table 2. Creutzfeldt-Jakob disease cases* in Texas by gender and age 2000–2006†§
Characteristics 2000 2001 2002 2003 2004 2005 2006 Total
Gender
Male 10 8 3 6 10 7 7 51
Female 4 6 4 10 3 8 2 37
Age (years)
<55>55 11 14 4 12 10 11 7 68
* Based on data as of June 15, 2007.
† Includes cases of possible, probable and confirmed sporadic CJD and confirmed familial CJD.
§ Based on year of death.
Volume 64/Number 8/ November 5, 2007
http://www.dshs.state.tx.us/idcu/epilink/volume_64/issue_8/docs/640804.pdf
please notice Texas 2006 ;
† Confirmed in United Kingdom and reported to Texas Department of State Health Services through Centers for Disease Control and Prevention.
Only 1 case of variant CJD has ever been diagnosed in Texas. The patient was a former resident of the United Kingdom, where the exposure was likely to have occurred. Texas has a population of 23 million, and since the national rate of sporadic CJD is about 1 per million, it is expected that approximately 23 cases of CJD would occur each year in the state. Therefore, it is believed that CJD is currently underreported in Texas. ...END...TSS
also see ;
http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/data/
Creutzfeldt-Jakob Disease in Northeast Texas,
J.A. Rawlings,*1 K.A. Hendricks1, O.M. Nuno1, D.A. Brown1, D.A. Evans2, Texas Department of Health, 1Austin and 2Tyler, Texas
Creutzfeldt-Jacob Disease (CJD), a transmissible spongiform encephalopathy, is caused by prions composed of proteinaceous material devoid of nucleic acid. CJD occurs sporadically (generally 1 case/1,000,000 population per year) in older patients (average age of 65) and is characterized by rapidly progressive dementia, accompanied by severe muscle spasms and incoordination. Death usually occurs within 3 to 12 months (average 7 months). CJD activity in Texas, which has a population of nearly 19 million, appeared to be typical. The statewide death rate for 1995 and 1996 was just under 1/1,000,000. In April of 1997, the Texas Department of Health became aware of an increased number of possible CJD cases in a 23-county area of NE Texas with a population of just over one million. After review of medical and pathology records, four patients were identified with definite classic CJD and three were identified with probable CJD. Dates of death for the eight patients were from April, 1996 through mid-July 1997. The patients were from 46 through 65 years of age; four were male and three were female. A case-control study to identify risks for CJD in NE Texas has been initiated.
http://www.jifsan.umd.edu/tse/Rawlings.htm
North American Equity Research
New York
13 January 2004
BSE (Mad Cow) Update:
Do Reports of sCJD Clusters Matter?
· There have been seven cases of human sCJD clusters identified in the US in the last 15 years, in which people in a specific location were diagnosed with sCJD, resulting in rates between 2.1 and 8.4 deaths per million people for that specific location compared with the national average of one in 1 million. · There is no proven link between sCJD and BSE, and hence it is considered a different disease from vCJD (which has been linked to BSE). However, the existence of clusters raises the question of “contamination" or “infection”, and also raises the hypothesis that rather than cases of sCJD these might have been cases of vCJD. · Clusters are not spontaneous, they normally have a source. Moreover, some cases of sCJD may have been improperly diagnosed as Alzheimer's.· We continue to believe that as long as no further cases of BSE-positive cows are found in North America and the industry has respected the 1997 ban on animal feed for live cattle, beef consumption in the US will not suffer. · Moreover, due to political pressure we expect key overseas markets (Japan, South Korea, and Mexico) to open up to US beef in the next six months – the recent 20% drop in cattle prices can be attributed mainly to these import bans. · However, two concerns linger and should be kept in mind by investors, 1) Has the 1997 ban on animal feed for live cattle been honored by the beef industry? 2) Can clusters of cases of sporadic CJD (or sCJD) really be a variant of CJD and indeed be linked to BSE? In this note we focus on the issue of sCJD clusters, and the potential impact that the growing debate on clusters could have on beef consumption in the US. United States Foods Pablo E. Zuanic(1-212) 622-6744pablo.zuanic@jpmorgan.comChristopher M. Bledsoe(1-212) 622-6386christopher.m.bledsoe@jpmorgan.comDaniel Ogbonna(212) 622-6382daniel.c.ogbonna@jpmorgan.com
State of Our Views Regarding BSE in the US
snip...
Existence of Clusters of sCJD May Imply They Are Really Cases of vCJD There have been seven sCJD clusters identified in the US in the last 15 years, in which people in a specific location were diagnosed with sCJD, resulting in rates between 1.2 and 8.4 deaths per million people for that specific location compared with the national average of one in 1 million. The existence of clusters raises the question of “contamination" or “infection”, and also raises the hypothesis that rather than cases of sCJD these might have been cases of vCJD. Clusters are not spontaneous, they normally have a source.
A cluster consists of two statistical improbabilities: 1) multiple cases occurring in a relatively limited geographic area, and 2) multiple cases occurring within the same time period. The most recent cluster was found in Cherry Hill, New Jersey. The others have been found in Lehigh, Pennsylvania (1986-90), Allentown, Pennsylvania (1989-92), Tampa, Florida (1996-97), Oregon (2001-02), and Nassau County, New York (1999-2000). Given that sCJD occurs randomly in one out of one million cases, it is a statistical rarity to find an sCJD cluster – let alone six. The following tables highlight known clusters in the US.
Table 1:
Clustered sCJD Deaths
Local sCJD Deaths
Time Span State Local Area Pop. (MM) Period (mo.) Total Ann'lized
1986-1990 PA Lehigh Valley 0.5 48 18 4.5
1989-1992 PA Allentown 2.5 36 15 5.0
1996-1997 FL Tampa 2.2 18 13 8.7
1996-1999 TX Denton .01 38 4 1.3
1999-2000 NY Nassau County 1.3 12 7 7.0
2001-2002 OR Entire State 3.4 24 14 7.0
2000-2003* NJ Cherry Hill Area 1.7 36 12 4.0
Source: JPMorgan.
The second table, below, shows what portion of the state's total expected sCJD cases (as based on a one per million occurrence) were found in the local cluster, comparing the local cluster's portion of cases with the local area's portion of the state's total population. The greater the factor between the former and the latter suggests a higher statistical improbability that the cluster is spontaneous (sCJD).
Table 2: Clustered sCJD Deaths vs. Expected State Cases
Annual Statewide Local Area (% of Time Span State Local Area sCJD Deaths* exp. state cases state pop.
1986-1990 PA Lehigh Valley 11.9 37.8% 4.5%
1989-1992 PA Allentown 12.0 41.7% 20.8%
1996-1997 FL Tampa 14.1 61.5% 15.7%
1996-1999 TX Denton 20.9 6.1% .02%
1999-2000 NY Nassau County 18.1 38.7% 7.4%
2001-2002 OR Entire State 3.4 205.9% 100.0%
2000-2003* NJ Cherry Hill Area 8.0 50.0% 21.6%
* *State cases are extrapolated based on state population and the 1 per million national average. Source: JPMorgan.
snip...
Copyright 2003 J.P. Morgan Chase & Co.—All rights reserved.
THIS MATERIAL IS ISSUED AND DISTRIBUTED IN MALAYSIA BY J.P. MORGAN MALAYSIA SDN. BHD. (18146-X).
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
https://lists.aegee.org/cgi-bin/wa?A2=ind0401&L=BSE-L&T=0&F=&S=&P=25337
JOURNAL OF NEUROLOGY
MARCH 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
flounder@wt.net
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535
US Concern CJD Screening May Miss Thousands Of Cases
By Steve Mitchell Zwire.co, United Press International (via COMTEX) 7-23-3
The UK Department of Health website maintains the only comprehensive source of comparative data on the incidence of the various forms of CJD in any population. The UK Department of Health monthly reports are reproduced in ProMED-mail close to the beginning of each month (see references below). - Mod.CP]
The federal government's monitoring system for cases of Creutzfeldt-Jakob disease (CJD), a fatal human brain illness, could be missing tens of thousands of victims, scientists and consumer advocates have told United Press International.
Variant CJD [abbreviated as CJD (new var.) or vCJD in ProMED-mail] can be [contracted] by eating beef [from cattle] with mad cow disease (bovine spongiform encephalopathy - abbreviated as BSE), but the critics assert that, without a better tracking system, it might be impossible to determine whether any [cases of sporadic CJD] are [cases of vCJD] or to obtain an accurate picture of the prevalence of the disorder in the United States.
Beginning in the late 1990s, more than 100 people contracted vCJD in the United Kingdom and several European countries after eating beef infected with BSE. [The mode of transmission of the BSE agent to humans has not been established conclusively, but is presumed on circumstantial grounds to be a consequence of consumption of contaminated meat. - Mod.CP]
No case of [BSE] has ever been detected in U.S. cattle, and the monitoring system of the Centers for Disease Control and Prevention (CDC) has never detected a case of vCJD . Nevertheless, critics say, the CDC's system [may] miss many cases of the disease, which currently is not treatable and is always fatal.
The first symptoms of CJD typically include memory loss and difficulty keeping balance and walking. As the disease destroys the brain, patients rapidly progress in a matter of months to difficulty with movement, an inability to talk and swallow and, finally, death. Spontaneously-occurring or sporadic CJD is a rare disorder. Only about 300 cases appear nationwide each year, but several studies have suggested that the disorder might be more common than thought and that as many as tens of thousands of cases might be going unrecognized. Clusters of [sporadic] CJD have been reported in various areas of the United States -- Pennsylvania in 1993, Florida in 1994, Oregon in 1996, New York in 1999-2000, and Texas in 1996. In addition, several people in New Jersey developed CJD in recent years, including a 56-year-old woman who died on 31 May 2003. Although in some instances, a [BSE] link was suspected, all of the cases ultimately were classified as sporadic CJD.
People who develop CJD [presumably as a result of] eating BSE-contaminated beef have been thought to develop the specific form of the disorder called variant CJD. But new research, released in December 2002 [see ProMED-mail post archived as: CJD (new var.) - UK: update 2003 (03) 20030204.0299], [suggests] that the [BSE] pathogen [may] cause both sporadic CJD and the variant form. "Now people are beginning to realize that because something looks like sporadic CJD they can't necessarily conclude that it is not linked to [BSE]," said Laura Manuelidis, section chief of surgery in the neuropathology department at Yale University, who conducted a 1989 study that found 13 percent of Alzheimer's patients actually had CJD.
Several studies, including the Manuelidis study, have found that autopsies reveal 3 to 13 percent of patients diagnosed with Alzheimer's or dementia actually suffered from CJD. Those numbers might sound low, but there are 4 million Alzheimer's cases and hundreds of thousands of dementia cases in the United States. A small percentage of those cases could add up to 120 000 or more CJD victims going undetected and not included in official statistics.
Experiences in [the UK] and Switzerland -- both countries that discovered mad cow disease in their cattle -- have heightened concerns about the possibility that some cases of sporadic CJD are due to consuming mad-cow-tainted beef. Both countries have reported increases in sporadic CJD since BSE was first detected in British herds in 1986. Switzerland discovered in 2002 that its CJD rate was twice that of any other country in the world. Switzerland had been seeing 8 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.
The CDC says the annual rate of CJD in the United States is one case per million people, but the above studies suggest the true prevalence of CJD is not known, Manuelidis told UPI. Diagnosing CJD or Alzheimer's is difficult because no test exists that can identify either disease in a living patient with certainty. So physicians must rely on the patient's symptoms to determine which illness might be present. Sometimes, however, the symptoms of one disease can appear similar to the other. The only way to determine the disease conclusively is to perform an autopsy on the brain after death. Unfortunately, although autopsies once were performed on approximately half of all corpses, the frequency has dropped to 15 percent or less in the United States. The National Center for Health Statistics (NCHS) -- a branch of the CDC -- stopped collecting autopsy data in 1995. "If we don't do autopsies and we don't look at people's brains ... we have no idea about the general prevalence of these kinds of infections and (whether) it is changing," Manuelidis said.
While autopsies have been declining, the number of deaths attributed to Alzheimer's has increased more than 50-fold since 1979, going from 857 deaths then to nearly 50 000 in 2000. Though it is unlikely the dramatic increase in Alzheimer's is due entirely to misdiagnosed CJD cases, it "could explain some of the increase we've seen," Manuelidis said.
"Neurodegenerative disease and Alzheimer's disease have become a waste-basket" for mental illness in the elderly that is difficult to diagnose conclusively, she said. "In other words, what people call Alzheimer's now is [broader] than what people used to call it, and that has the possibility of encompassing more diseases -- including CJD." The autopsy studies that found undiagnosed CJD cases raise the question of whether the United States "already has an undetected epidemic here," Jeff Nelson, director of Vegsource.com, a vegetarian advocacy web-site, told UPI. "What's the source of that?" Nelson asked. "Could it be the same source of encephalopathy we saw in minks?"
Nelson referred to an outbreak of a [transmissible spongiform encephalopathy] in minks in Wisconsin in the 1980s. The origin was traced back to the animals' diet, which included parts of so-called downer cattle -- sick cows that are unable to stand, which often indicates a neurological disease, including mad cow. The mink disease raised concerns about whether U.S. cattle were carrying a mad-cow-like pathogen even prior to the U.K. epidemic that began in 1986.
Andrew Monjan, chief of the neuropsychology of aging program at the National Institute of Aging (part of the National Institutes of Health in Bethesda, Maryland), acknowledged there has been an increase in U.S. Alzheimer's cases. However, he told UPI, this probably is due to the aging of the population -- as people grow older, they develop a higher risk of developing Alzheimer's. "There's been no change in the number of CJD cases in the country, and there has been clearly a tracking of the unusual cases of CJD" that could be due to mad cow disease, Monjan said.
However, Terry Singletary, coordinator of CJD Watch -- an organization founded to track CJD cases -- says efforts to track the disease have been close to nonexistent. For example, only 12 states require such reports. Therefore, many cases might be going undetected, unreported, or misdiagnosed. If more states made CJD a reportable illness, there would be more clusters detected across the United States, said Singletary, who became involved with CJD advocacy after his mother died from a form of CJD known as Heidenhain variant.
In the 18-year period between 1979 and 1996, he noted, the country saw a jump from one case of sporadic CJD in people under the age of 30 -- a warning sign for a link to [BSE], because nearly all of the U.K. victims were 30 years of age or younger, to 5 cases in 5 years between 1997 and 2001. "That represents a substantial blip," he told UPI. Singletary also said there have been increases in sporadic CJD in France, Germany, and Italy, all of which have detected mad cow disease in their cattle.
So far, the CDC has refused to impose a national requirement that physicians and hospitals report cases of the disease. The agency has not chosen to make CJD a reportable disease because "making it reportable is not necessarily directly helpful in surveillance, because in some states where it's reportable you may not get the physician to report it," said Dr. Ermias Belay, CDC's medical epidemiologist working on CJD. Instead, the agency relies on other methods, including death certificates and urging physicians to send suspicious cases to the National Prion Disease Pathology Surveillance Center (NPDPSC) at Case Western Reserve University in Cleveland, which is funded by the CDC.
However, because autopsies generally are not done, if a CJD case is misdiagnosed as Alzheimer's or dementia, a correct diagnosis might never be made, and therefore the cause of death listed on a death certificate might be inaccurate. Belay told UPI he discounted this possibility. It is unlikely to happen, he said, because it is easy to distinguish CJD from Alzheimer's -- the 2 conditions display different symptoms.
Manuelidis disagreed. It can be quite difficult to determine accurately whether a patient has CJD, as evidenced by her study, in which respected and competent neurologists and psychiatrists at Yale originally diagnosed patients with Alzheimer's, yet were wrong at least 13 percent of the time. Another study conducted at the University of Pennsylvania, which found 6 percent of dementia patients actually were suffering from CJD, supports the difficulty in distinguishing the illnesses correctly. The U. Penn. researchers concluded that: "These results show that in patients with a clinical diagnosis of dementia, the etiology cannot be accurately predicted during life."
In addition, the NPDPSC sees less than half of all the CJD cases each year, so the CDC's investigational system not only is missing many of the misdiagnosed CJD cases, it also is not conducting autopsies on most of the detected cases. Belay said that the CDC follows up on all cases of CJD that occur in people under age 55, as these could be linked to variant (BSE-related) CJD. But so far, all have turned out to be sporadic forms of the disease. About 30 cases of the disorder occur each year in the United States in this age group, while the remaining 270 or so are older.
The case of a Philadelphia woman who developed a brain disorder that appeared to be CJD and died from it in 2000 at the age of 29 -- illustrates just how difficult it can be to diagnose the disease. Her physician, Dr. Peter Crinos of the University of Pennsylvania Medical Center, ruled out other disorders and felt certain the young woman had died of CJD, a concern that raised the possibility of a link to mad cow disease because of her young age. When neuropathologist Nicholas Gonatas, who had seen CJD before, examined the woman's brain after her death, he, likewise, was confident he detected the microscopic, sponge-like holes caused by the disease. But when he sent brain samples to the NPDPSC, the results came back negative. Gonatas, convinced the surveillance center's finding was erroneous, sent off 2 more samples, only to have them both come back negative. Subsequent research, however, has shown the test used by the surveillance center cannot rule out CJD, said Crinos, an assistant professor of neurology. "There's no question that the young woman had a spongiform encephalopathy," Crinos said, but added although it appeared to be CJD, it is difficult if not impossible to say whether it was due to mad cow disease.
Crinos told UPI until the CDC implements a better tracking system, a lot of questions will remain about CJD and cases like the young Philadelphia woman's. One central question: Why are cases of what is presumed to be a rare disease popping up in clusters in certain areas of the country? Crinos said the clustering suggests an environmental or food-borne cause, but so far, "No one knows the answer to that."
http://www.zwire.com/site/news.cfm?newsid=9882702&BRD=1713&PAG=740&dept_id=226965&rfi=6
ProMED Mail promed@promedmail.org
[The above article raises some significant issues related to CJD surveillance in the USA, and factors that may be contributing to a significant under-reporting of CJD cases. First and foremost, CJD is not a nationally reportable disease. Even with nationally reportable diseases, one sees significant under-reporting, probably related to the health care delivery system in the USA, which is heavily weighted towards private-sector providers. Unfortunately the private sector is less consistent with disease reporting to state and federal levels. In the absence of a national mandate for reporting of a disease, the incentive becomes negligible, so the traditional "tip of the iceberg" seen in disease reporting shrinks even further.
The study suggesting that up to 13 percent of cases diagnosed with Alzheimer's and other dementias may be due to CJD points out another weak link in CJD surveillance. The diagnosis does necessitate an autopsy, and autopsy rates have declined markedly in the USA, especially in the elderly. Hence the "Catch 22" -- what is needed for the diagnosis is an autopsy, but the autopsy isn't performed (as has been the case in many of the CJD "cluster" reports). The reverse of "seek and ye shall find" is "don't look and the problem isn't there." - Mod.MPP]
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
http://cjdusa.blogspot.com/
CJD QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/
SCRAPIE USA
http://scrapie-usa.blogspot.com/
NOR-98 ATYPICAL SCRAPIE CASES USA
http://nor-98.blogspot.com/
CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA
http://cjdmadcowbaseoct2007.blogspot.com/
Transmissible Mink Encephalopathy TME
http://transmissible-mink-encephalopathy.blogspot.com/
CHRONIC WASTING DISEASE
http://chronic-wasting-disease.blogspot.com/
TSEAC MEETING
----- Original Message -----
From: Terry S. Singeltary Sr.
To: FREAS@CBER.FDA.GOVCc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
Sent: Wednesday, November 29, 2006 1:24 PM
Subject: TSE advisory committee for the meeting December 15, 2006 [TSSSUBMISSION]
November 29, 2006
Greetings FDA, DHH, Dr. Freas, and Dr. Harvey et al,
a kind and warm Holiday Greetings to you all. i kindly wish to submit the following to the TSE advisory committee for the meeting December 15, 2006, about the assessment for potential exposure to vCJD in human plasma-derived antihemophilic factor (FVIII) products manufactured from U.S. plasma donors and related communication material ;
http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-20251.htm
i see the media picked up on this as a 'low risk', from what the gov. agency perceived to be to them;
http://www.newsday.com/news/health/ats-ap_health14nov27,0,7955259.story?coll=ny-leadhealthnews-headlines
however, i seem to disagree. from my primitive ciphering, i see it anotherway. this is a huge catastrophic risk. 3 in 160 is 1.9%. so call that 2% which is 1 in 50 or twenty per thousand or 20,000 per million. also, what about the mixed genotypes/mixed susceptibility? what about the silent carriers that donated tainted blood? what about the sporadic CJDs of UNKNOWN strain or phenotype? this risk assessment is just more BSe to me. just another in a long line of ...
Greetings again Dr. Freas et al at FDA,
THIS was like closing the barn door after the mad cows got loose. not only the red cross, but the FDA has failed the public in protecting them from the TSE aka madcow agent. TSE agent i.e. bse, base, cwd, scrapie, tme, and any sub strains thereof. we do not know if these strains will or have transmitted to humans as subclinical TSE or clinical disease, and we do not know if they have or will transmit second, third, forth passage via friendly fire i.e. multiple potential routes via medical, surgical, pharmaceutical etc. IF you remember correctly Dr. Freas et al, i called this long ago, almost 6 years ago ;
PDF]Freas, William TSS SUBMISSION Terry S. Singeltary Sr. [flounder@wt.net] Monday, January 08, 200l 3:03 PM freas ...Freas, William From: Terry S. Singeltary Sr. [flounder@wt.net] Sent: Monday, January 08,200l 3:03 PM To: freas@CBS5055530.CBER.FDA.GOV
Subject: CJD/BSE (aka madcow) Human/Animal TSE?s--U.S.--Submission
To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products.
snip...
I am beginning to think that the endless attempt to track down and ban, potential victims from known BSE Countries from giving blood will be futile. You would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT SWIFTLY to find blood test for TSE's, whether it be blood test, urine test, eyelid test, anything at whatever cost, we need a test FAST. DO NOT let the incubation time period of these TSEs fool you. To think of Scrapie as the prime agent to compare CJD, but yet overlook the Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by scrapie from a vaccine made of scrapie infected sheep brains, would be foolish. I acquired this full text version of the event which was recorded in the Annual Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. From the BVA and the URL is posted in my (long version). ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
see full text ;
http://tseac.blogspot.com/
vCJD case study highlights blood transfusion risk
http://vcjdblood.blogspot.com/
Wednesday, October 24, 2007
MADCOW USDA the untold story
http://madcowusda.blogspot.com/
FOIA MAD SHEEP MAD RIVER VALLEY
DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [Docket No. 00-072-1]
http://foiamadsheepmadrivervalley.blogspot.com/
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle
9/13/2005
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
SEAC 99 DECEMBER 14, 2007
Conclusions
14. Preliminary research findings suggest that the potential risk of transmission of vCJD via dental procedures may be greater than previously anticipated. Although this research is incomplete, uses an animal model exposed to relatively high doses of infectivity, and there are no data from infectivity studies on human oral tissues, these findings suggest an increased possibility that vCJD may be relatively efficiently transmitted via a range of dental procedures. Ongoing infectivity studies using human oral tissues and the other studies suggested here will enable more precise assessment of the risks of vCJD transmission through dental procedures.
15. Guidance was issued to dentists earlier this year recommending that endodontic files and reamers be treated as single use which, provided it is adhered to, will remove any risk of a self-sustaining epidemic arising from re-use of these instruments. To minimise risk it is critical that appropriate management and audit is in place, both for NHS and private dentistry.
16. It is also critical that a detailed and comprehensive assessment of the risks of all dental procedures be conducted as a matter of urgency. While taking into account the continuing scientific uncertainties, this will allow a more thorough consideration of the possible public health implications of vCJD transmission via dentistry and the identification of possible additional precautionary risk reduction measures. The assessment will require continued updating as more evidence becomes available on the transmissibility of vCJD by dental routes, and on the prevalence of infection within the population. A DH proposal to convene an expert group that includes dental professionals to expedite such an assessment is welcomed. Given the potential for transmission via dentistry, consideration should be given to the urgent assessment of new decontamination technologies which, if proved robust and effective, could significantly reduce transmission risks.
SEAC June 2007
27 SEAC Epidemiology Subgroup (2006) position statement of the vCJD epidemic.
http://www.seac.gov.uk/statements/state260106subgroup.htm
28 DH (2007) Precautionary advice given to dentists on re-use of instruments
http://www.gnn.gov.uk/environment/fullDetail.asp?ReleaseID=279256&NewsAreaID=2&NavigatedFromDepartment=False
see full text 17 pages ;
http://www.seac.gov.uk/papers/99-7.pdf
SEAC 99th meeting on Friday 14th December 2007
DECEMBER 14, 2007, 10 year Anniversary of my Moms death 'confirmed' from Heidenhain Variant Creutzfeldt Jakob Disease
Greetings,
AS one of them _lay_ folks, one must only ponder ;
"WITH the Nor-98 now documented in five different states so far in the USA in 2007, and with the TWO atypical BSE H-BASE cases in Texas and Alabama, with both scrapie and CWD running rampant in the USA, IS there any concern from SEAC with the rise of sporadic CJD in the USA from ''UNKNOWN PHENOTYPE'', and what concerns if any, in relations to blood donations, surgery, optical, and dental, do you have with these unknown atypical phenotypes in both humans and animals in the USA ???"
"Does it concern SEAC, or is it of no concern to SEAC?"
"Should it concern USA animal and human health officials?"
snip...
----- Original Message -----
From: xxxxxxxxxx
To: flounder9@verizon.net
Sent: Thursday, November 22, 2007 5:39 AM
Subject: QUESTION FOR SEAC
Mr Terry S Singeltary Sr., Bacliff, Texas 77518 USA.
Dear Mr Singeltary,
"Thank you for your e-mail of yesterday with the question for SEAC. I can confirm that this will be asked at the meeting on your behalf and the question and answer will appear in the minutes of the meeting which will be published on the SEAC Internet site."
snip...end...TSS
Archive Number 20071105.3602 Published Date 05-NOV-2007 Subject PRO/AH/EDR> Prion disease update 2007 (07)
PRION DISEASE UPDATE 2007 (07)
****************************** A ProMED-mail post
snip...
[2] USA: National Prion Disease Pathology Surveillance Center Date: June 2007 Source: National Prion Disease Pathology Surveillance Center (USA) [edited]
CJD Cases examined ---------------------- Year / Referrals / Prion disease / Sporadic / Familial / Iatrogenic / vCJD
1996 / 42 / 32 / 26 / 4 / 0 / 0
1997 / 115 / 68 / 57 / 9 / 0 / 0
1998 / 93 / 53 / 45 / 7 / 1 / 0
1999 / 114 / 69 / 61 / 8 / 0 / 0
2000 / 151 / 103 / 89 / 14 / 0 / 0
2001 / 208 / 116 / 106 / 9 / 0 / 0
2002 / 255 / 143 / 118 / 23 / 2 / 0
2003 / 272 / 174 / 132 / 41 / 0 / 0
2004 / 334 / 183 / 157 / 21 / 0 / 1*
2005 / 352 / 195 / 152 / 37 / 1 / 0
2006 / 372 / 186 / 143 / 30 / 0 / 1**
2007 / 120 / 68 / 35 / 7 / 0 / 0
TOTAL / 2428*** / 1390**** / 1121 / 210 / 4 / 2
*Acquired in UK
** Acquired in Saudi Arabia
*** Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007.
**** Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1
from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36
type pending (2 from 2005, 8 from 2006, 26 from 2007).
Notes:
-- Cases are listed based on the year of death when available. If the year of death is not available, the year of sample receipt is used.
-- Referrals: Cases with possible or probable prion disease from which brain tissue or blood in the case of familial disease were submitted.
-- Inconclusive: Cases in which the samples were not sufficient to make a diagnosis.
-- Non-vCJD type unknown are cases in which the tissue submitted was adequate to establish the presence but not the type; in all cases, vCJD could be excluded.
-- Communicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963
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.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
snip...full text ;
http://seac992007.blogspot.com/
Sunday, December 16, 2007
Risk factors for sporadic Creutzfeldt-Jakob disease
Published Online: 11 Dec 2007
Copyright © 2007 American Neurological Association
Original Article
Risk factors for sporadic Creutzfeldt-Jakob disease
Hester J. T. Ward, FFPH 1 *, Dawn Everington, MSc 1, Simon N. Cousens, MA 2, Blaire Smith-Bathgate, RGN 1, Michelle Gillies, MRCP 1, Katy Murray, MRCP 1, Richard S. G. Knight, FRCPE 1, Peter G. Smith, DSc 2, Robert G. Will, FRCP 1 1National Creutzfeldt-Jakob Disease Surveillance Unit, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom 2Department of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London, United Kingdom
email: Hester J. T. Ward (h.ward@ed.ac.uk)
*Correspondence to Hester J. T. Ward, National CJD Surveillance Unit, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, United Kingdom
Funded by: Department of Health; Grant Number: 121/7400 Scottish Executive Health Department; Grant Number: R39924
Abstract
Objective
Although surgical transmission of Creutzfeldt-Jakob disease (CJD) has been demonstrated, these iatrogenic cases account for only a small proportion of all CJD cases. The majority are sporadic CJD (sCJD) cases of unknown cause. This study investigated whether some cases classified as sCJD might have an unrecognized iatrogenic basis through surgical or other medical procedures
Methods
This study compared medical risk factors from 431 sCJD cases referred 1998 to 2006 with 454 population control subjects. Possible geographic and temporal links between neurological and gynecological operations in 857 sCJD cases referred from 1990 to 2006 were investigated
Results
A reported history of ever having undergone surgery was associated with increased risk for sCJD (odds ratio, 2.0; 95% confidence interval, 1.3-2.1; p = 0.003). Increased risk was not associated with surgical categories chosen a priori but was confined to the residual category other surgery, in which the increase in risk appeared most marked for three subcategories: skin stitches, nose/throat operations, and removal of growths/cysts/moles. No convincing evidence was found of links (same hospital, within 2 years) between cases undergoing neurosurgery or gynecological surgery
Interpretation
It is unlikely that a high proportion of UK sCJD cases are the result of transmission during surgery, but we cannot exclude the possibility that such transmission occurs occasionally. A study based on accurate surgical histories obtained from medical records is required to determine whether the increased risk associated with reported surgical history reflects a causal association or recall bias. Ann Neurol 2007
----------------------------------------------------------------------------
Received: 24 May 2007; Revised: 5 September 2007; Accepted: 1 October 2007 Digital Object Identifier (DOI)
10.1002/ana.21294 About DOI
Additional Material
http://www3.interscience.wiley.com/cgi-bin/abstract/117861913/ABSTRACT?CRETRY=1&SRETRY=0
***
which the increase in risk appeared most marked for three subcategories:
skin stitches, nose/throat operations, and removal of growths/cysts/moles.
10 January 1990
Other US BSE risks: the imported products picture
24 Jul 00 Trade Statistics: UK to US
Compiled by Terry S. Singeltary Sr of Bacliff, Texas
[Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep. This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human medicines. What has become of these?
Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.
Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]
* which the increase in risk appeared most marked for three subcategories:
* skin stitches, nose/throat operations, and removal of growths/cysts/moles.
10 January 1990
Other US BSE risks: the imported products picture
24 Jul 00 Trade Statistics: UK to US
Compiled by Terry S. Singeltary Sr of Bacliff, Texas
[Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep. This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human medicines. What has become of these?
Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.
Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]
10 January 1990
NOT FOR PUBLICATION
COMMITTEE ON SAFETY OF MEDICINES
WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY
SURGICAL CATGUT SUTURES
2.1 At the first meeting of the Working Party on Bovine Spongiform Encephalopathy on 6 September 1989, detailed consideration was given to XXXXX Surgical Catgut. This arose from the Company's response to the Letter to License Holders, indicating that the bovine small intestine source material was derived from UK cattle, unlike 8 other licensed catgut sutures. In contrast XXXXX Surgical Catgut was stated to hold over 90% share of the market for catgut sutures, and to constitute approximately 83% of all sutures used in U.K.
IMPORTS OF SUTURES FROM THE KNOWN BSE COUNTRY;
snip... please see full text ;
http://creutzfeldt-jakob-disease.blogspot.com/
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Creutzfeldt-Jakob Disease Surveillance in Texas 2000–2006
Abstract
Creutzfeldt-Jakob disease (CJD) is a rare neurodegenerative disease caused by prions. The disease is usually fatal within a year and there is currently no known treatment or cure. CJD has been a reportable condition in Texas since 1998. There are currently four known types: sporadic, familial, variant, and iatrogenic. Diagnosis is complex and direct examination of brain tissue is required for case confirmation and identification of the type of CJD. During 2000–2006, there were 181 cases of confirmed, probable, or possible CJD diagnosed among Texas residents, including 88 cases of sporadic CJD, 5 cases of familial CJD, and 1 case of variant CJD. Most case-patients were male (55%) and 55 years of age or older (78%). The Texas Department of State Health Services is available to assist health care professionals with arrangement of free diagnostic testing and to provide resources for family support.
snip...
Texas Surveillance
CJD has been a reportable condition in Texas since 1998. The majority of CJD cases are reported to the Texas Department of State Health Services (DSHS) by test or autopsy reports received from the Prion Center. A few cases are discovered by routine death certificate review and some cases are reported by a local or regional health department, health care provider, or family member. Copies of results from all CJD-related testing performed by the Prion Center are sent to DSHS as a part of routine surveillance procedures. DSHS reviews test results and investigates all cases with positive test results including those with elevated CSF 14-3-3 protein levels. Table 1 summarizes the number of cases for all types of CJD in Texas (2000–2006). Each year in Texas, the total number of confirmed, probable, or possible sporadic CJD cases has remained somewhat constant (mean=13; range= 6–15). In addition, on average, one case of familial CJD was diagnosed each year in Texas during 2000–2006, all from separate families. Only 1 case of variant CJD has ever been diagnosed in Texas. The patient was a former resident of the United Kingdom, where the exposure was likely to have occurred. Texas has a population of 23 million, and since the national rate of sporadic CJD is about 1 per million, it is expected that approximately 23 cases of CJD would occur each year in the state. Therefore, it is believed that CJD is currently underreported in Texas. Table 2 describes sporadic and familial CJD cases in Texas according to gender and age. Of the patients diagnosed with CJD during 2000–2006, 58% were male and 79% were 55 years of age or older. Figure 1 depicts the number of CJD cases per county for the years 2000–2006. Note that higher numbers of cases are located in counties with higher populations.
CJD should be suspected and reported to DSHS in individuals who meet the following criteria:
1) Dementia of early onset (younger than 55 years of age) or 2) Rapidly progressive dementia and one of more of the following: • Movement disorder • Painful sensory symptoms • Visual disturbances or 3) Diagnosed by a physician as having CJD
Case Classification
The World Health Organization (WHO) established recommended standards for all types of CJD surveillance in 1997 (Table 3). The United States, including Texas, has adopted these surveillance standards to determine case classification for sCJD, fCJD and iCJD. For vCJD, CDC has developed diagnostic case criteria for use in the United States (Table 3). Direct examination of brain tissue through either biopsy or autopsy is highly recommended for all types of CJD and is required for confirmation of sporadic CJD and variant CJD. A sCJD case is determined to be ‘probable’ if there is enough diagnostic testing to suggest CJD but no autopsy has been performed. Patients considered for
probable sCJD must exhibit progressive dementia and have a typical EEG and/or elevated CSF 14-3-3 protein. In addition they must display at least 2 of 4 clinical features: myoclonus, visual or cerebellar disturbance, akinetic mutism, and/or pyramidal/extrapyramidal dysfunction. For a case to be listed as ‘possible’, the patient must have progressive dementia and at least 2 of the listed clinical features, disease duration of less than 2 years and either no EEG testing or EEG atypical for CJD. Iatrogenic CJD must have a known risk factor, e.g., high risk surgery or cadaver-derived pituitary hormone. Familial CJD is considered confirmed in a patient with a neuropsychiatric disorder if a first degree relative had confirmed or probable CJD or a disease-specific prion protein gene mutation has been identified. Table 3 describes the case classification for each type of CJD.
Conclusions
CJD is an emerging disease that may be misdiagnosed and appears to be underreported in Texas. As with other emerging diseases, the partnership of the medical community and public health epidemiologists provides a framework to share information and expertise among local, state, federal and international colleagues and to detect and respond to
diseases that are rapidly fatal, difficult to diagnose, and rare. Enhanced surveillance will provide a better understanding of the epidemiology of this disease and its impact and opportunities for mitigation. Recognition of possible CJD and reporting by health professionals is an integral part of CJD surveillance in Texas. CJD is a reportable disease in Texas. All suspected cases should be reported within one week to the Texas Department of State Health Services, Infectious Disease Control Unit. Confirmation and typing of the disease requires neuropathological confirmation by direct examination of brain tissue, usually postmortem, by the Prion Center. It is important to establish the precise type of CJD to help monitor disease occurrence especially for variant CJD. Physicians should strongly consider arranging for autopsies of suspected or clinically-diagnosed CJD patients. The Texas Department of State Health Services can assist health professionals by arranging free diagnostic testing and providing resources for family support.
References...snip...end...TSS
Table 1. Cases of Creutzfeldt-Jakob disease in Texas*§
Type 2000 2001 2002 2003 2004 2005 2006 Total
Sporadic
Confirmed 9 8 4 6 7 8 5 47
Probable 2 4 1 5 5 6 3 26
Possible 3 1 1 4 1 0 0 10
Subtotal 14 13 6 15 13 14 8 83
Familial 0 1 1 1 0 1 1 5
Iatrogenic 0 0 0 0 0 0 0 0
Variant 0 0 0 0 0 0 1† 1
Total 14 14 7 16 13 15 10 89
*Based on data as of June 15, 2007.
† Confirmed in United Kingdom and reported to Texas Department of State Health Services through Centers for Disease Control and Prevention.
§ Based on year of death.
Table 2. Creutzfeldt-Jakob disease cases* in Texas by gender and age 2000–2006†§
Characteristics 2000 2001 2002 2003 2004 2005 2006 Total
Gender
Male 10 8 3 6 10 7 7 51
Female 4 6 4 10 3 8 2 37
Age (years)
<55>55 11 14 4 12 10 11 7 68
* Based on data as of June 15, 2007.
† Includes cases of possible, probable and confirmed sporadic CJD and confirmed familial CJD.
§ Based on year of death.
Volume 64/Number 8/ November 5, 2007
http://www.dshs.state.tx.us/idcu/epilink/volume_64/issue_8/docs/640804.pdf
please notice Texas 2006 ;
† Confirmed in United Kingdom and reported to Texas Department of State Health Services through Centers for Disease Control and Prevention.
Only 1 case of variant CJD has ever been diagnosed in Texas. The patient was a former resident of the United Kingdom, where the exposure was likely to have occurred. Texas has a population of 23 million, and since the national rate of sporadic CJD is about 1 per million, it is expected that approximately 23 cases of CJD would occur each year in the state. Therefore, it is believed that CJD is currently underreported in Texas. ...END...TSS
also see ;
http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/data/
Creutzfeldt-Jakob Disease in Northeast Texas,
J.A. Rawlings,*1 K.A. Hendricks1, O.M. Nuno1, D.A. Brown1, D.A. Evans2, Texas Department of Health, 1Austin and 2Tyler, Texas
Creutzfeldt-Jacob Disease (CJD), a transmissible spongiform encephalopathy, is caused by prions composed of proteinaceous material devoid of nucleic acid. CJD occurs sporadically (generally 1 case/1,000,000 population per year) in older patients (average age of 65) and is characterized by rapidly progressive dementia, accompanied by severe muscle spasms and incoordination. Death usually occurs within 3 to 12 months (average 7 months). CJD activity in Texas, which has a population of nearly 19 million, appeared to be typical. The statewide death rate for 1995 and 1996 was just under 1/1,000,000. In April of 1997, the Texas Department of Health became aware of an increased number of possible CJD cases in a 23-county area of NE Texas with a population of just over one million. After review of medical and pathology records, four patients were identified with definite classic CJD and three were identified with probable CJD. Dates of death for the eight patients were from April, 1996 through mid-July 1997. The patients were from 46 through 65 years of age; four were male and three were female. A case-control study to identify risks for CJD in NE Texas has been initiated.
http://www.jifsan.umd.edu/tse/Rawlings.htm
North American Equity Research
New York
13 January 2004
BSE (Mad Cow) Update:
Do Reports of sCJD Clusters Matter?
· There have been seven cases of human sCJD clusters identified in the US in the last 15 years, in which people in a specific location were diagnosed with sCJD, resulting in rates between 2.1 and 8.4 deaths per million people for that specific location compared with the national average of one in 1 million. · There is no proven link between sCJD and BSE, and hence it is considered a different disease from vCJD (which has been linked to BSE). However, the existence of clusters raises the question of “contamination" or “infection”, and also raises the hypothesis that rather than cases of sCJD these might have been cases of vCJD. · Clusters are not spontaneous, they normally have a source. Moreover, some cases of sCJD may have been improperly diagnosed as Alzheimer's.· We continue to believe that as long as no further cases of BSE-positive cows are found in North America and the industry has respected the 1997 ban on animal feed for live cattle, beef consumption in the US will not suffer. · Moreover, due to political pressure we expect key overseas markets (Japan, South Korea, and Mexico) to open up to US beef in the next six months – the recent 20% drop in cattle prices can be attributed mainly to these import bans. · However, two concerns linger and should be kept in mind by investors, 1) Has the 1997 ban on animal feed for live cattle been honored by the beef industry? 2) Can clusters of cases of sporadic CJD (or sCJD) really be a variant of CJD and indeed be linked to BSE? In this note we focus on the issue of sCJD clusters, and the potential impact that the growing debate on clusters could have on beef consumption in the US. United States Foods Pablo E. Zuanic(1-212) 622-6744pablo.zuanic@jpmorgan.comChristopher M. Bledsoe(1-212) 622-6386christopher.m.bledsoe@jpmorgan.comDaniel Ogbonna(212) 622-6382daniel.c.ogbonna@jpmorgan.com
State of Our Views Regarding BSE in the US
snip...
Existence of Clusters of sCJD May Imply They Are Really Cases of vCJD There have been seven sCJD clusters identified in the US in the last 15 years, in which people in a specific location were diagnosed with sCJD, resulting in rates between 1.2 and 8.4 deaths per million people for that specific location compared with the national average of one in 1 million. The existence of clusters raises the question of “contamination" or “infection”, and also raises the hypothesis that rather than cases of sCJD these might have been cases of vCJD. Clusters are not spontaneous, they normally have a source.
A cluster consists of two statistical improbabilities: 1) multiple cases occurring in a relatively limited geographic area, and 2) multiple cases occurring within the same time period. The most recent cluster was found in Cherry Hill, New Jersey. The others have been found in Lehigh, Pennsylvania (1986-90), Allentown, Pennsylvania (1989-92), Tampa, Florida (1996-97), Oregon (2001-02), and Nassau County, New York (1999-2000). Given that sCJD occurs randomly in one out of one million cases, it is a statistical rarity to find an sCJD cluster – let alone six. The following tables highlight known clusters in the US.
Table 1:
Clustered sCJD Deaths
Local sCJD Deaths
Time Span State Local Area Pop. (MM) Period (mo.) Total Ann'lized
1986-1990 PA Lehigh Valley 0.5 48 18 4.5
1989-1992 PA Allentown 2.5 36 15 5.0
1996-1997 FL Tampa 2.2 18 13 8.7
1996-1999 TX Denton .01 38 4 1.3
1999-2000 NY Nassau County 1.3 12 7 7.0
2001-2002 OR Entire State 3.4 24 14 7.0
2000-2003* NJ Cherry Hill Area 1.7 36 12 4.0
Source: JPMorgan.
The second table, below, shows what portion of the state's total expected sCJD cases (as based on a one per million occurrence) were found in the local cluster, comparing the local cluster's portion of cases with the local area's portion of the state's total population. The greater the factor between the former and the latter suggests a higher statistical improbability that the cluster is spontaneous (sCJD).
Table 2: Clustered sCJD Deaths vs. Expected State Cases
Annual Statewide Local Area (% of Time Span State Local Area sCJD Deaths* exp. state cases state pop.
1986-1990 PA Lehigh Valley 11.9 37.8% 4.5%
1989-1992 PA Allentown 12.0 41.7% 20.8%
1996-1997 FL Tampa 14.1 61.5% 15.7%
1996-1999 TX Denton 20.9 6.1% .02%
1999-2000 NY Nassau County 18.1 38.7% 7.4%
2001-2002 OR Entire State 3.4 205.9% 100.0%
2000-2003* NJ Cherry Hill Area 8.0 50.0% 21.6%
* *State cases are extrapolated based on state population and the 1 per million national average. Source: JPMorgan.
snip...
Copyright 2003 J.P. Morgan Chase & Co.—All rights reserved.
THIS MATERIAL IS ISSUED AND DISTRIBUTED IN MALAYSIA BY J.P. MORGAN MALAYSIA SDN. BHD. (18146-X).
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
https://lists.aegee.org/cgi-bin/wa?A2=ind0401&L=BSE-L&T=0&F=&S=&P=25337
JOURNAL OF NEUROLOGY
MARCH 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
flounder@wt.net
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535
US Concern CJD Screening May Miss Thousands Of Cases
By Steve Mitchell Zwire.co, United Press International (via COMTEX) 7-23-3
The UK Department of Health website maintains the only comprehensive source of comparative data on the incidence of the various forms of CJD in any population. The UK Department of Health monthly reports are reproduced in ProMED-mail close to the beginning of each month (see references below). - Mod.CP]
The federal government's monitoring system for cases of Creutzfeldt-Jakob disease (CJD), a fatal human brain illness, could be missing tens of thousands of victims, scientists and consumer advocates have told United Press International.
Variant CJD [abbreviated as CJD (new var.) or vCJD in ProMED-mail] can be [contracted] by eating beef [from cattle] with mad cow disease (bovine spongiform encephalopathy - abbreviated as BSE), but the critics assert that, without a better tracking system, it might be impossible to determine whether any [cases of sporadic CJD] are [cases of vCJD] or to obtain an accurate picture of the prevalence of the disorder in the United States.
Beginning in the late 1990s, more than 100 people contracted vCJD in the United Kingdom and several European countries after eating beef infected with BSE. [The mode of transmission of the BSE agent to humans has not been established conclusively, but is presumed on circumstantial grounds to be a consequence of consumption of contaminated meat. - Mod.CP]
No case of [BSE] has ever been detected in U.S. cattle, and the monitoring system of the Centers for Disease Control and Prevention (CDC) has never detected a case of vCJD . Nevertheless, critics say, the CDC's system [may] miss many cases of the disease, which currently is not treatable and is always fatal.
The first symptoms of CJD typically include memory loss and difficulty keeping balance and walking. As the disease destroys the brain, patients rapidly progress in a matter of months to difficulty with movement, an inability to talk and swallow and, finally, death. Spontaneously-occurring or sporadic CJD is a rare disorder. Only about 300 cases appear nationwide each year, but several studies have suggested that the disorder might be more common than thought and that as many as tens of thousands of cases might be going unrecognized. Clusters of [sporadic] CJD have been reported in various areas of the United States -- Pennsylvania in 1993, Florida in 1994, Oregon in 1996, New York in 1999-2000, and Texas in 1996. In addition, several people in New Jersey developed CJD in recent years, including a 56-year-old woman who died on 31 May 2003. Although in some instances, a [BSE] link was suspected, all of the cases ultimately were classified as sporadic CJD.
People who develop CJD [presumably as a result of] eating BSE-contaminated beef have been thought to develop the specific form of the disorder called variant CJD. But new research, released in December 2002 [see ProMED-mail post archived as: CJD (new var.) - UK: update 2003 (03) 20030204.0299], [suggests] that the [BSE] pathogen [may] cause both sporadic CJD and the variant form. "Now people are beginning to realize that because something looks like sporadic CJD they can't necessarily conclude that it is not linked to [BSE]," said Laura Manuelidis, section chief of surgery in the neuropathology department at Yale University, who conducted a 1989 study that found 13 percent of Alzheimer's patients actually had CJD.
Several studies, including the Manuelidis study, have found that autopsies reveal 3 to 13 percent of patients diagnosed with Alzheimer's or dementia actually suffered from CJD. Those numbers might sound low, but there are 4 million Alzheimer's cases and hundreds of thousands of dementia cases in the United States. A small percentage of those cases could add up to 120 000 or more CJD victims going undetected and not included in official statistics.
Experiences in [the UK] and Switzerland -- both countries that discovered mad cow disease in their cattle -- have heightened concerns about the possibility that some cases of sporadic CJD are due to consuming mad-cow-tainted beef. Both countries have reported increases in sporadic CJD since BSE was first detected in British herds in 1986. Switzerland discovered in 2002 that its CJD rate was twice that of any other country in the world. Switzerland had been seeing 8 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.
The CDC says the annual rate of CJD in the United States is one case per million people, but the above studies suggest the true prevalence of CJD is not known, Manuelidis told UPI. Diagnosing CJD or Alzheimer's is difficult because no test exists that can identify either disease in a living patient with certainty. So physicians must rely on the patient's symptoms to determine which illness might be present. Sometimes, however, the symptoms of one disease can appear similar to the other. The only way to determine the disease conclusively is to perform an autopsy on the brain after death. Unfortunately, although autopsies once were performed on approximately half of all corpses, the frequency has dropped to 15 percent or less in the United States. The National Center for Health Statistics (NCHS) -- a branch of the CDC -- stopped collecting autopsy data in 1995. "If we don't do autopsies and we don't look at people's brains ... we have no idea about the general prevalence of these kinds of infections and (whether) it is changing," Manuelidis said.
While autopsies have been declining, the number of deaths attributed to Alzheimer's has increased more than 50-fold since 1979, going from 857 deaths then to nearly 50 000 in 2000. Though it is unlikely the dramatic increase in Alzheimer's is due entirely to misdiagnosed CJD cases, it "could explain some of the increase we've seen," Manuelidis said.
"Neurodegenerative disease and Alzheimer's disease have become a waste-basket" for mental illness in the elderly that is difficult to diagnose conclusively, she said. "In other words, what people call Alzheimer's now is [broader] than what people used to call it, and that has the possibility of encompassing more diseases -- including CJD." The autopsy studies that found undiagnosed CJD cases raise the question of whether the United States "already has an undetected epidemic here," Jeff Nelson, director of Vegsource.com, a vegetarian advocacy web-site, told UPI. "What's the source of that?" Nelson asked. "Could it be the same source of encephalopathy we saw in minks?"
Nelson referred to an outbreak of a [transmissible spongiform encephalopathy] in minks in Wisconsin in the 1980s. The origin was traced back to the animals' diet, which included parts of so-called downer cattle -- sick cows that are unable to stand, which often indicates a neurological disease, including mad cow. The mink disease raised concerns about whether U.S. cattle were carrying a mad-cow-like pathogen even prior to the U.K. epidemic that began in 1986.
Andrew Monjan, chief of the neuropsychology of aging program at the National Institute of Aging (part of the National Institutes of Health in Bethesda, Maryland), acknowledged there has been an increase in U.S. Alzheimer's cases. However, he told UPI, this probably is due to the aging of the population -- as people grow older, they develop a higher risk of developing Alzheimer's. "There's been no change in the number of CJD cases in the country, and there has been clearly a tracking of the unusual cases of CJD" that could be due to mad cow disease, Monjan said.
However, Terry Singletary, coordinator of CJD Watch -- an organization founded to track CJD cases -- says efforts to track the disease have been close to nonexistent. For example, only 12 states require such reports. Therefore, many cases might be going undetected, unreported, or misdiagnosed. If more states made CJD a reportable illness, there would be more clusters detected across the United States, said Singletary, who became involved with CJD advocacy after his mother died from a form of CJD known as Heidenhain variant.
In the 18-year period between 1979 and 1996, he noted, the country saw a jump from one case of sporadic CJD in people under the age of 30 -- a warning sign for a link to [BSE], because nearly all of the U.K. victims were 30 years of age or younger, to 5 cases in 5 years between 1997 and 2001. "That represents a substantial blip," he told UPI. Singletary also said there have been increases in sporadic CJD in France, Germany, and Italy, all of which have detected mad cow disease in their cattle.
So far, the CDC has refused to impose a national requirement that physicians and hospitals report cases of the disease. The agency has not chosen to make CJD a reportable disease because "making it reportable is not necessarily directly helpful in surveillance, because in some states where it's reportable you may not get the physician to report it," said Dr. Ermias Belay, CDC's medical epidemiologist working on CJD. Instead, the agency relies on other methods, including death certificates and urging physicians to send suspicious cases to the National Prion Disease Pathology Surveillance Center (NPDPSC) at Case Western Reserve University in Cleveland, which is funded by the CDC.
However, because autopsies generally are not done, if a CJD case is misdiagnosed as Alzheimer's or dementia, a correct diagnosis might never be made, and therefore the cause of death listed on a death certificate might be inaccurate. Belay told UPI he discounted this possibility. It is unlikely to happen, he said, because it is easy to distinguish CJD from Alzheimer's -- the 2 conditions display different symptoms.
Manuelidis disagreed. It can be quite difficult to determine accurately whether a patient has CJD, as evidenced by her study, in which respected and competent neurologists and psychiatrists at Yale originally diagnosed patients with Alzheimer's, yet were wrong at least 13 percent of the time. Another study conducted at the University of Pennsylvania, which found 6 percent of dementia patients actually were suffering from CJD, supports the difficulty in distinguishing the illnesses correctly. The U. Penn. researchers concluded that: "These results show that in patients with a clinical diagnosis of dementia, the etiology cannot be accurately predicted during life."
In addition, the NPDPSC sees less than half of all the CJD cases each year, so the CDC's investigational system not only is missing many of the misdiagnosed CJD cases, it also is not conducting autopsies on most of the detected cases. Belay said that the CDC follows up on all cases of CJD that occur in people under age 55, as these could be linked to variant (BSE-related) CJD. But so far, all have turned out to be sporadic forms of the disease. About 30 cases of the disorder occur each year in the United States in this age group, while the remaining 270 or so are older.
The case of a Philadelphia woman who developed a brain disorder that appeared to be CJD and died from it in 2000 at the age of 29 -- illustrates just how difficult it can be to diagnose the disease. Her physician, Dr. Peter Crinos of the University of Pennsylvania Medical Center, ruled out other disorders and felt certain the young woman had died of CJD, a concern that raised the possibility of a link to mad cow disease because of her young age. When neuropathologist Nicholas Gonatas, who had seen CJD before, examined the woman's brain after her death, he, likewise, was confident he detected the microscopic, sponge-like holes caused by the disease. But when he sent brain samples to the NPDPSC, the results came back negative. Gonatas, convinced the surveillance center's finding was erroneous, sent off 2 more samples, only to have them both come back negative. Subsequent research, however, has shown the test used by the surveillance center cannot rule out CJD, said Crinos, an assistant professor of neurology. "There's no question that the young woman had a spongiform encephalopathy," Crinos said, but added although it appeared to be CJD, it is difficult if not impossible to say whether it was due to mad cow disease.
Crinos told UPI until the CDC implements a better tracking system, a lot of questions will remain about CJD and cases like the young Philadelphia woman's. One central question: Why are cases of what is presumed to be a rare disease popping up in clusters in certain areas of the country? Crinos said the clustering suggests an environmental or food-borne cause, but so far, "No one knows the answer to that."
http://www.zwire.com/site/news.cfm?newsid=9882702&BRD=1713&PAG=740&dept_id=226965&rfi=6
ProMED Mail promed@promedmail.org
[The above article raises some significant issues related to CJD surveillance in the USA, and factors that may be contributing to a significant under-reporting of CJD cases. First and foremost, CJD is not a nationally reportable disease. Even with nationally reportable diseases, one sees significant under-reporting, probably related to the health care delivery system in the USA, which is heavily weighted towards private-sector providers. Unfortunately the private sector is less consistent with disease reporting to state and federal levels. In the absence of a national mandate for reporting of a disease, the incentive becomes negligible, so the traditional "tip of the iceberg" seen in disease reporting shrinks even further.
The study suggesting that up to 13 percent of cases diagnosed with Alzheimer's and other dementias may be due to CJD points out another weak link in CJD surveillance. The diagnosis does necessitate an autopsy, and autopsy rates have declined markedly in the USA, especially in the elderly. Hence the "Catch 22" -- what is needed for the diagnosis is an autopsy, but the autopsy isn't performed (as has been the case in many of the CJD "cluster" reports). The reverse of "seek and ye shall find" is "don't look and the problem isn't there." - Mod.MPP]
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
http://cjdusa.blogspot.com/
CJD QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/
SCRAPIE USA
http://scrapie-usa.blogspot.com/
NOR-98 ATYPICAL SCRAPIE CASES USA
http://nor-98.blogspot.com/
CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA
http://cjdmadcowbaseoct2007.blogspot.com/
Transmissible Mink Encephalopathy TME
http://transmissible-mink-encephalopathy.blogspot.com/
CHRONIC WASTING DISEASE
http://chronic-wasting-disease.blogspot.com/
TSEAC MEETING
----- Original Message -----
From: Terry S. Singeltary Sr.
To: FREAS@CBER.FDA.GOVCc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
Sent: Wednesday, November 29, 2006 1:24 PM
Subject: TSE advisory committee for the meeting December 15, 2006 [TSSSUBMISSION]
November 29, 2006
Greetings FDA, DHH, Dr. Freas, and Dr. Harvey et al,
a kind and warm Holiday Greetings to you all. i kindly wish to submit the following to the TSE advisory committee for the meeting December 15, 2006, about the assessment for potential exposure to vCJD in human plasma-derived antihemophilic factor (FVIII) products manufactured from U.S. plasma donors and related communication material ;
http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-20251.htm
i see the media picked up on this as a 'low risk', from what the gov. agency perceived to be to them;
http://www.newsday.com/news/health/ats-ap_health14nov27,0,7955259.story?coll=ny-leadhealthnews-headlines
however, i seem to disagree. from my primitive ciphering, i see it anotherway. this is a huge catastrophic risk. 3 in 160 is 1.9%. so call that 2% which is 1 in 50 or twenty per thousand or 20,000 per million. also, what about the mixed genotypes/mixed susceptibility? what about the silent carriers that donated tainted blood? what about the sporadic CJDs of UNKNOWN strain or phenotype? this risk assessment is just more BSe to me. just another in a long line of ...
Greetings again Dr. Freas et al at FDA,
THIS was like closing the barn door after the mad cows got loose. not only the red cross, but the FDA has failed the public in protecting them from the TSE aka madcow agent. TSE agent i.e. bse, base, cwd, scrapie, tme, and any sub strains thereof. we do not know if these strains will or have transmitted to humans as subclinical TSE or clinical disease, and we do not know if they have or will transmit second, third, forth passage via friendly fire i.e. multiple potential routes via medical, surgical, pharmaceutical etc. IF you remember correctly Dr. Freas et al, i called this long ago, almost 6 years ago ;
PDF]Freas, William TSS SUBMISSION Terry S. Singeltary Sr. [flounder@wt.net] Monday, January 08, 200l 3:03 PM freas ...Freas, William From: Terry S. Singeltary Sr. [flounder@wt.net] Sent: Monday, January 08,200l 3:03 PM To: freas@CBS5055530.CBER.FDA.GOV
Subject: CJD/BSE (aka madcow) Human/Animal TSE?s--U.S.--Submission
To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products.
snip...
I am beginning to think that the endless attempt to track down and ban, potential victims from known BSE Countries from giving blood will be futile. You would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT SWIFTLY to find blood test for TSE's, whether it be blood test, urine test, eyelid test, anything at whatever cost, we need a test FAST. DO NOT let the incubation time period of these TSEs fool you. To think of Scrapie as the prime agent to compare CJD, but yet overlook the Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by scrapie from a vaccine made of scrapie infected sheep brains, would be foolish. I acquired this full text version of the event which was recorded in the Annual Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. From the BVA and the URL is posted in my (long version). ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
see full text ;
http://tseac.blogspot.com/
vCJD case study highlights blood transfusion risk
http://vcjdblood.blogspot.com/
Wednesday, October 24, 2007
MADCOW USDA the untold story
http://madcowusda.blogspot.com/
FOIA MAD SHEEP MAD RIVER VALLEY
DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [Docket No. 00-072-1]
http://foiamadsheepmadrivervalley.blogspot.com/
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle
9/13/2005
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
SEAC 99 DECEMBER 14, 2007
Conclusions
14. Preliminary research findings suggest that the potential risk of transmission of vCJD via dental procedures may be greater than previously anticipated. Although this research is incomplete, uses an animal model exposed to relatively high doses of infectivity, and there are no data from infectivity studies on human oral tissues, these findings suggest an increased possibility that vCJD may be relatively efficiently transmitted via a range of dental procedures. Ongoing infectivity studies using human oral tissues and the other studies suggested here will enable more precise assessment of the risks of vCJD transmission through dental procedures.
15. Guidance was issued to dentists earlier this year recommending that endodontic files and reamers be treated as single use which, provided it is adhered to, will remove any risk of a self-sustaining epidemic arising from re-use of these instruments. To minimise risk it is critical that appropriate management and audit is in place, both for NHS and private dentistry.
16. It is also critical that a detailed and comprehensive assessment of the risks of all dental procedures be conducted as a matter of urgency. While taking into account the continuing scientific uncertainties, this will allow a more thorough consideration of the possible public health implications of vCJD transmission via dentistry and the identification of possible additional precautionary risk reduction measures. The assessment will require continued updating as more evidence becomes available on the transmissibility of vCJD by dental routes, and on the prevalence of infection within the population. A DH proposal to convene an expert group that includes dental professionals to expedite such an assessment is welcomed. Given the potential for transmission via dentistry, consideration should be given to the urgent assessment of new decontamination technologies which, if proved robust and effective, could significantly reduce transmission risks.
SEAC June 2007
27 SEAC Epidemiology Subgroup (2006) position statement of the vCJD epidemic.
http://www.seac.gov.uk/statements/state260106subgroup.htm
28 DH (2007) Precautionary advice given to dentists on re-use of instruments
http://www.gnn.gov.uk/environment/fullDetail.asp?ReleaseID=279256&NewsAreaID=2&NavigatedFromDepartment=False
see full text 17 pages ;
http://www.seac.gov.uk/papers/99-7.pdf
SEAC 99th meeting on Friday 14th December 2007
DECEMBER 14, 2007, 10 year Anniversary of my Moms death 'confirmed' from Heidenhain Variant Creutzfeldt Jakob Disease
Greetings,
AS one of them _lay_ folks, one must only ponder ;
"WITH the Nor-98 now documented in five different states so far in the USA in 2007, and with the TWO atypical BSE H-BASE cases in Texas and Alabama, with both scrapie and CWD running rampant in the USA, IS there any concern from SEAC with the rise of sporadic CJD in the USA from ''UNKNOWN PHENOTYPE'', and what concerns if any, in relations to blood donations, surgery, optical, and dental, do you have with these unknown atypical phenotypes in both humans and animals in the USA ???"
"Does it concern SEAC, or is it of no concern to SEAC?"
"Should it concern USA animal and human health officials?"
snip...
----- Original Message -----
From: xxxxxxxxxx
To: flounder9@verizon.net
Sent: Thursday, November 22, 2007 5:39 AM
Subject: QUESTION FOR SEAC
Mr Terry S Singeltary Sr., Bacliff, Texas 77518 USA.
Dear Mr Singeltary,
"Thank you for your e-mail of yesterday with the question for SEAC. I can confirm that this will be asked at the meeting on your behalf and the question and answer will appear in the minutes of the meeting which will be published on the SEAC Internet site."
snip...end...TSS
Archive Number 20071105.3602 Published Date 05-NOV-2007 Subject PRO/AH/EDR> Prion disease update 2007 (07)
PRION DISEASE UPDATE 2007 (07)
****************************** A ProMED-mail post
snip...
[2] USA: National Prion Disease Pathology Surveillance Center Date: June 2007 Source: National Prion Disease Pathology Surveillance Center (USA) [edited]
CJD Cases examined ---------------------- Year / Referrals / Prion disease / Sporadic / Familial / Iatrogenic / vCJD
1996 / 42 / 32 / 26 / 4 / 0 / 0
1997 / 115 / 68 / 57 / 9 / 0 / 0
1998 / 93 / 53 / 45 / 7 / 1 / 0
1999 / 114 / 69 / 61 / 8 / 0 / 0
2000 / 151 / 103 / 89 / 14 / 0 / 0
2001 / 208 / 116 / 106 / 9 / 0 / 0
2002 / 255 / 143 / 118 / 23 / 2 / 0
2003 / 272 / 174 / 132 / 41 / 0 / 0
2004 / 334 / 183 / 157 / 21 / 0 / 1*
2005 / 352 / 195 / 152 / 37 / 1 / 0
2006 / 372 / 186 / 143 / 30 / 0 / 1**
2007 / 120 / 68 / 35 / 7 / 0 / 0
TOTAL / 2428*** / 1390**** / 1121 / 210 / 4 / 2
*Acquired in UK
** Acquired in Saudi Arabia
*** Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007.
**** Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1
from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36
type pending (2 from 2005, 8 from 2006, 26 from 2007).
Notes:
-- Cases are listed based on the year of death when available. If the year of death is not available, the year of sample receipt is used.
-- Referrals: Cases with possible or probable prion disease from which brain tissue or blood in the case of familial disease were submitted.
-- Inconclusive: Cases in which the samples were not sufficient to make a diagnosis.
-- Non-vCJD type unknown are cases in which the tissue submitted was adequate to establish the presence but not the type; in all cases, vCJD could be excluded.
-- Communicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963
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.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
snip...full text ;
http://seac992007.blogspot.com/
Sunday, December 16, 2007
Risk factors for sporadic Creutzfeldt-Jakob disease
Published Online: 11 Dec 2007
Copyright © 2007 American Neurological Association
Original Article
Risk factors for sporadic Creutzfeldt-Jakob disease
Hester J. T. Ward, FFPH 1 *, Dawn Everington, MSc 1, Simon N. Cousens, MA 2, Blaire Smith-Bathgate, RGN 1, Michelle Gillies, MRCP 1, Katy Murray, MRCP 1, Richard S. G. Knight, FRCPE 1, Peter G. Smith, DSc 2, Robert G. Will, FRCP 1 1National Creutzfeldt-Jakob Disease Surveillance Unit, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom 2Department of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London, United Kingdom
email: Hester J. T. Ward (h.ward@ed.ac.uk)
*Correspondence to Hester J. T. Ward, National CJD Surveillance Unit, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, United Kingdom
Funded by: Department of Health; Grant Number: 121/7400 Scottish Executive Health Department; Grant Number: R39924
Abstract
Objective
Although surgical transmission of Creutzfeldt-Jakob disease (CJD) has been demonstrated, these iatrogenic cases account for only a small proportion of all CJD cases. The majority are sporadic CJD (sCJD) cases of unknown cause. This study investigated whether some cases classified as sCJD might have an unrecognized iatrogenic basis through surgical or other medical procedures
Methods
This study compared medical risk factors from 431 sCJD cases referred 1998 to 2006 with 454 population control subjects. Possible geographic and temporal links between neurological and gynecological operations in 857 sCJD cases referred from 1990 to 2006 were investigated
Results
A reported history of ever having undergone surgery was associated with increased risk for sCJD (odds ratio, 2.0; 95% confidence interval, 1.3-2.1; p = 0.003). Increased risk was not associated with surgical categories chosen a priori but was confined to the residual category other surgery, in which the increase in risk appeared most marked for three subcategories: skin stitches, nose/throat operations, and removal of growths/cysts/moles. No convincing evidence was found of links (same hospital, within 2 years) between cases undergoing neurosurgery or gynecological surgery
Interpretation
It is unlikely that a high proportion of UK sCJD cases are the result of transmission during surgery, but we cannot exclude the possibility that such transmission occurs occasionally. A study based on accurate surgical histories obtained from medical records is required to determine whether the increased risk associated with reported surgical history reflects a causal association or recall bias. Ann Neurol 2007
----------------------------------------------------------------------------
Received: 24 May 2007; Revised: 5 September 2007; Accepted: 1 October 2007 Digital Object Identifier (DOI)
10.1002/ana.21294 About DOI
Additional Material
http://www3.interscience.wiley.com/cgi-bin/abstract/117861913/ABSTRACT?CRETRY=1&SRETRY=0
***
which the increase in risk appeared most marked for three subcategories:
skin stitches, nose/throat operations, and removal of growths/cysts/moles.
10 January 1990
Other US BSE risks: the imported products picture
24 Jul 00 Trade Statistics: UK to US
Compiled by Terry S. Singeltary Sr of Bacliff, Texas
[Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep. This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human medicines. What has become of these?
Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.
Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]
* which the increase in risk appeared most marked for three subcategories:
* skin stitches, nose/throat operations, and removal of growths/cysts/moles.
10 January 1990
Other US BSE risks: the imported products picture
24 Jul 00 Trade Statistics: UK to US
Compiled by Terry S. Singeltary Sr of Bacliff, Texas
[Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep. This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human medicines. What has become of these?
Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.
Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]
10 January 1990
NOT FOR PUBLICATION
COMMITTEE ON SAFETY OF MEDICINES
WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY
SURGICAL CATGUT SUTURES
2.1 At the first meeting of the Working Party on Bovine Spongiform Encephalopathy on 6 September 1989, detailed consideration was given to XXXXX Surgical Catgut. This arose from the Company's response to the Letter to License Holders, indicating that the bovine small intestine source material was derived from UK cattle, unlike 8 other licensed catgut sutures. In contrast XXXXX Surgical Catgut was stated to hold over 90% share of the market for catgut sutures, and to constitute approximately 83% of all sutures used in U.K.
IMPORTS OF SUTURES FROM THE KNOWN BSE COUNTRY;
snip... please see full text ;
http://creutzfeldt-jakob-disease.blogspot.com/
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
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