Organ distribution of prion proteins in variant Creutzfeldt-Jakob disease

The Lancet Infectious Diseases, Volume 3, Issue 4, Pages 214 - 222, April 2003

doi:10.1016/S1473-3099(03)00578-4Cite or Link Using DOI

Organ distribution of prion proteins in variant Creutzfeldt-Jakob disease

Original Text

Dr I Ramasamy a , M Law b, S Collins c, F Brook a

Summary

In this article we give an overview of the transmissible spongiform encephalopathies, with emphasis on the evidence for the distribution of abnormal prions in tissues. The normal prion protein is distributed ubiquitously throughout human body tissues. Endogenous expression of the normal prion protein, as well as auxiliary proteins, plays a part in accumulation of the abnormal prion protein. As exemplified by variant Creutzfeldt-Jakob disease (vCJD) the abnormal prion protein can accumulate in the host lymphoid system, in particular the follicular dendritic cells. The route for the disease-related prion neuroinvasion is likely to involve the peripheral nervous system. An alternative route may involve blood constituents. Both animal studies and studies on vCJD patients suggest a potential for abnormal prion distribution in several peripheral tissues other than the lymphoreticular system. In human beings the abnormal prion has been reported in the brain, tonsils, spleen, lymph node, retina, and proximal optic nerve. Infectivity, although present in peripheral tissues, is at lower levels than in the central nervous system (CNS). Animal models suggest that the growth of infectivity in the CNS is likely to be gradual with maximum values during the clinical phase of disease. That tissues may harbour the abnormal prion, at different levels of infectivity, during the incubation period of the disease raises concerns of iatrogenic transmission of the disease either after surgery, blood transfusion, or accidental organ transplantation from donors in the preclinical phase of the disease.


http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(03)00578-4/fulltext#article_upsell


Cadaver corneal transplants -- without family permission

Houston, Texas channel 11 news 28 Nov 99

Reported by Terry S. Singeltary Sr. son of CJD victim

"It was a story about how the Lions eye bank were harvesting corneas from victims in the Morgue, without their consent. Under Texas law, this appears to be legal (remember Texas has the Veggie liable law). Even if Family says no, this appears to happen, from what the news story said. They said the only way to prevent this, is to fill out a form, stating not to have this done. So if you don't fill out the form, they can do this. How many people don't know about the form?

This is not only disgusting and appalling, it could be highly infectious. Without proper background checking of the donors, on their physical history, checking on past dementia, and/or family history, some of these unfortunate victims, could be passing a human TSE.

Response Jill Spitler Clevelland Eye Bank:

"No, we are not stealing.........Yes, you do have such a law in the state of Texas, but not all your state Eye Banks utilize the law. The Eye Bank that you're speaking of is only one of 43 certified Eye Bank throughout the USA.

And there are measure taken per the Medical Standards of the Eye Bank Association of America, the certifying body for eye banks and per FDA regulations to address those concerns that you speak of.

I would suggest that those interested/concern with transplant contact their local agencies. The Eye Bank Association of America has a web. site . Further if anyone has problems contacting or finding out about their local organization(s), call me or e-mail me I would be glad to help. My e-mail address is jill@clevelandeyebank.org"

Terry Singeltary responds:

"Explain this to the family in Houston who went to their loved ones funeral, only to find out that the loved one that was in the casket, had their corneas removed without their permission, without the consent of the victim or it's family. They would not have known it, only for the funny look the victim had. So, they questioned, only to find out, the corneas, had in fact, been removed without consent.

I call that stealing, regardless what the law states. This type of legal grave robbing is not a logical thing to do without knowing any type of background of the victims medical past, which really will not prove anything due to the incubation period. Eye tissue being potentially a highly infective source, there are risks here.

Should they not at least know of the potential ramifications of TSE's (the person receiving the corneas)?

Should there not be some sort of screening?

Should there be some sort of moral issue here? If this is the case, and in fact, they can come take your corneas, without your consent, then what will they start taking next, without your consent?

Lets look at a hypothetical situation: What would happen if my Mom (DOD 12-14-97 hvCJD) would have gotten into a car wreck and died, before the symptoms of CJD appeared. Not much money, so there was no autopsy. What would have happened to that recipient of those infecting corneas?"

Comment (webmaster): Actual transmission of CJD by means of corneal transplant may or may not be rare. The incidence of infectivity in older people could be fairly high; this is not to be confused with the lower incidence of symptomatic (clinical) CJD. It is very unlikely that familial CJD would have been diagnosed in earlier generations; however, without interviewing the family even known kindreds would not be excluded.

In blood donation, a much stricter policy is followed, even though corneal transplant may be far more dangerous (being a direct link to the brain and not going through purification steps).

Since highly sensitive tests for pre-clinical CJD are now available, it would make sense to screen corneas for CJD, just as they are screened for AIDS, hepatitus, and a host of other conditions.


http://mad-cow.org/~tom/dec99_news.html#bbb


please see full text here ;

Monday, August 31, 2009

HUMAN BODY PARTS FOR SALE TO THE HIGHEST BIDDER Inside a Creepy Global Body Parts Business


http://creutzfeldt-jakob-disease.blogspot.com/2009/08/human-body-parts-for-sale-to-highest.html


THE LEGALITY OF STEALING ORGAN/TISSUE...

TEXAS STATUTES

Sec. 693.012. Removal of Corneal Tissue Permitted Under Certain Circumstances.

On a request from an authorized official of an eye bank for corneal tissue, a justice of the peace or medical examiner may permit the removal of corneal tissue if:

(1) the decedent from whom the tissue is to be removed died under circumstances requiring an inquest by the justice of the peace or medical examiner;

(2) no objection by a person listed in Section 693.013 is known by the justice of the peace or medical examiner; and

(3) the removal of the corneal tissue will not interfere with the subsequent course of an investigation or autopsy or alter the decedent's postmortem facial appearance.

Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.

Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.

Search 1999 Legislation for: 693.012

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TEXAS STATUTES Sec. 693.003. Consent Required in Certain Circumstances.

(a) A medical examiner or a person acting on the authority of a medical examiner may not remove a visceral organ unless the medical examiner or person obtains the consent of a person listed in Section 693.004.

(b) If a person listed in Section 693.004 is known and available within four hours after death is pronounced, a medical examiner or a person acting on the authority of a medical examiner may not remove a nonvisceral organ or tissue unless the medical examiner or person obtains that person's consent.

(c) If a person listed in Section 693.004 cannot be identified and contacted within four hours after death is pronounced and the medical examiner determines that no reasonable likelihood exists that a person can be identified and contacted during the four-hour period, the medical examiner may permit the removal of a nonvisceral organ or tissue.

Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.

Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.

Search 1999 Legislation for: 693.003

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PLEASE NOTE; the bottom would only pertain to those who know of the law. if you don't know about it, you cannot dispute, so in four hours, they can legally remove body organs, as long as they don't disfigure. and who is to know the difference? makes me wonder of some of my dead relatives, and if they were burried with their eye's and or any of their organs. This is very disturbing, if not for moral reasons, but for the risk of dangerous pathogens (human TSE's, etc.) to be transmitted. only time will tell, but i am very disturbed. these laws are not morally correct. They should be re-written as to they cannot so easily take your organs, with no one knowing. The Family or Victim, must consent. There should be some kind of research on donor/family medical history... TSS

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Sec. 693.013. Persons Who May Object to Removal.

The following persons may object to the removal of corneal tissue:

(1) the decedent's spouse;

(2) the decedent's adult children, if there is no spouse;

(3) the decedent's parents, if there is no spouse or adult child; or

(4) the decedent's brothers or sisters, if there is no spouse, adult child, or parent.

Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.

Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.

Search 1999 Legislation for: 693.013

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to cover one's butt....



Sec. 693.014. Immunity From Damages in Civil Action.

(a) In a civil action brought by a person listed in Section 693.013 who did not object before the removal of corneal tissue, a medical examiner, justice of the peace, or eye bank official is not liable for damages on a theory of civil recovery based on a contention that the person's consent was required before the corneal tissue could be removed.

(b) Chapter 104, Civil Practice and Remedies Code, applies to a justice of the peace, medical examiner, and their personnel who remove, permit removal, or deny removal of corneal tissue under this subchapter as if the justice of the peace, medical examiner, and their personnel were state officers or employees.

Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.

Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.

Search 1999 Legislation for: 693.014

[[[as you can see, they knew it was wrong when they wrote the laws. or they would not have covered the rear-ends so well...TSS]]]

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thanks again, kind regards, Terry S. Singeltary Sr.


############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############


full text ;

Saturday, January 26, 2008

CJD HGH BODY SNATCHERS


http://creutzfeldt-jakob-disease.blogspot.com/2008/01/cjd-hgh-body-snatchers.html



URGENT DATA ON ATYPICAL BSE RISK FACTORS TO HUMANS AND ANIMALS OIE REFUSE TO ACKNOWLEDGE $

position: Post Doctoral Fellow Atypical BSE in Cattle

Closing date: December 24, 2009

Anticipated start date: January/February 2010

Employer: Canadian and OIE Reference Laboratories for BSE CFIA Lethbridge Laboratory, Lethbridge/Alberta

snip...

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

snip...


http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2



please see full text ;

Wednesday, March 31, 2010

Atypical BSE in Cattle


http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.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/



Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009

snip...

I ask Professor Kong ;

Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment

''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''

Professor Kong reply ;

.....snip

''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete.

Thanks for your interest.''

Best regards,

Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA

END...TSS

I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS



http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html



TSS

Cases of Early-Onset Sporadic Creutzfeld-Jakob Disease in Michigan

Chronic Wasting Disease and Potential Transmission to Humans

Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,† Michael W. Miller,‡ Pierluigi Gambetti,§ and Lawrence B. Schonberger*

snip...

In 2001, two additional CJD patients 26 and 28 years of age were reported from a single state (Table 2) (34). The patients grew up in adjacent counties and had illness onset within several months of each other. As a result of this fact and their unusually young age, a possible environmental source of infection, including exposure to CWD-infected venison, was considered. One of the patients died after an illness lasting 5–6 months that was characterized by progressive aphasia, memory loss, social withdrawal, vision disturbances, and seizure activity leading to status epilepticus and induced coma. Histopathologic, immunohistochemical, and Western blot testing of brain biopsy and autopsy samples confirmed a CJD diagnosis. The patient’s disease phenotype corresponded to the MM2 sporadic CJD subtype reported by Parchi et al. (35). This patient did not hunt, and family members provided no history of regularly eating venison. The patient may have occasionally eaten venison originating from the Upper Peninsula of Michigan while away from home during his college years. However, ongoing surveillance has not detected CWD in Michigan deer (36).

The second patient died from an illness lasting ˜16 months. The patient’s illness began with behavioral changes, including unusual outbursts of anger and depression. Confusion, memory loss, gait disturbances, incontinence, headaches, and photophobia also developed. Western blot analysis of frozen brain biopsy tissue confirmed a prion disease diagnosis. Immunohistochemical analysis of brain tissue obtained after the patient’s death

showed prion deposition consistent with GSS. Aprion protein gene analysis could not be performed because appropriate samples were lacking. However, prion protein gene analysis of a blood sample from one of the patient’s parents indicated a GSS P102L mutation. The patient did not hunt but may have eaten venison from Michigan once when he was 1–2 years old. The GSS diagnosis greatly reduced the likelihood that the two patients reported from adjacent counties had disease with a common origin. Recently, rare neurologic disorders resulting in the deaths of three men who participated in “wild game feasts” in a cabin owned by one of the decedents created concern about the possible relationship of their illnesses with CWD (Table 2) (37). Two of the patients reportedly died of CJD, and the third died from Pick’s disease. More than 50 persons were identified as possibly participating in these feasts; the three patients were the only participants reported to have died of a degenerative neurologic disorder. Reanalysis of autopsy brain tissues from the three patients at the National Prion Disease Pathology Surveillance Center indicated that two of them had no evidence of a prion disease by immunohistochemical analysis. CJD was confirmed in the third patient, who had clinicopathologic, codon 129, and prion characteristics similar to the most common sporadic CJD subtype (MM1/MV1) (35). This patient participated in the feasts only once, perhaps in the mid-1980s. In addition, the investigation found no evidence that the deer and elk meat served during the feasts originated from the known CWD-endemic areas of Colorado and Wyoming.

In 2003, CJD in two deer and elk hunters (54 and 66 years of age) was reported (38). The report implied that the patients had striking neuropathologic similarities and that their illness may represent a new entity in the spectrum of prion diseases. A third patient (63 years of age), who was also purported to have been a big game hunter, was subsequently reported from the same area. However, none of the three patients were reported to have eaten venison from the CWD-endemic areas of the western United States. The 66- year-old patient hunted most of his life in Washington State. Although information about the 54-year-old patient was limited, there was no evidence that he hunted in CWD-endemic areas. The third patient was not a hunter but ate venison harvested from Pennsylvania and Washington. The neuropathologic changes, Western blot profile, and genotype at codon 129 of the three patients each fit the MM1, VV1, or VV2 sporadic CJD subtype, indicating absence of phenotypic similarity among the cases or atypical neuropathologic features (35). To date, only two nonfamilial CJD cases with a positive history of exposure to venison obtained from the known CWD-endemic areas have been reported. One of the patients was a 61-year-old woman who grew up in an area where this disease is known to be endemic, and she ate venison harvested locally. She died in 2000, and analysis of autopsy brain specimens confirmed that the patient’s CJD phenotype fit the MM1 subtype, with no atypical neuropathologic features. The second patient was a 66-yearold man who was reported to have eaten venison from two deer harvested in a CWD-endemic area. Both deer tested negative for CWD, and the patient’s illness was consistent with the MM1 CJD phenotype.




http://www.cdc.gov/ncidod/EID/vol10no6/pdfs/03-1082.pdf




Archive Number 20020430.4061

Published Date 30-APR-2002

Subject PRO/AH/EDR> CJD, sporadic? - USA (Michigan)

CJD, SPORADIC? - USA (MICHIGAN)

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A ProMED-mail post

<http://www.promedmail.org>

ProMED-mail is a program of the International Society for Infectious Diseases <http://www.isid.org>

[see also: CJD (new var.), suspected - USA (FL) ex UK 20020419.3989 CJD (new var.) - UK: update Apr 2002 20020404.3877 CJD (new var.) - France: sixth case 20020418.3983 CJD (new var.), suspected case - Italy (Sicily) (03) 20020210.3528 CJD (new var.) - China (Hong Kong): confirmed 20020222.3604 2001 ---- Chronic wasting disease, cervid - USA: human risk? 20010126.0193 CJD (new var.), incidence & trends - UK 20011115.2816 CJD (new var.), incidence & trends - UK (02) 20011124.2875 CJD (new var.) - UK: 9th Annual Report 20010706.1293 CJD (new var.) - UK: regional variation 20010628.1231 CJD (new var.) - UK: regional variation (02) 20010907.2145 1999 ---- CJD (new var.), human - Ireland 19990715.1192]

[1] Date: Sat, 27 Apr 2002 20:28:05 -0400 From: Terry Allen <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000043/!x-usc:mailto:tallen@igc.org>

Source: Abstract presented at American Academy of Neurology meeting, Denver, 13-20 Apr 2002

Cases of Early-Onset Sporadic Creutzfeld-Jakob Disease in Michigan

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

Amanda C. Peltier, Patience H. Reading, Karen Kluin, SharinSakurai, Ahmad Beydoun, Jonathan Edwards, Pierluigi Gambetti, Norman L. Foster Ann Arbor , MI; Cleveland, OH

OBJECTIVE: To describe the clinical, pathological and genetic features in 2 young men who developed sporadic Creutzfeldt-Jakob disease (CJD) concurrently in Michigan.

BACKGROUND: Sporadic CJD typically occurs in the 6th and 7th decades of life and is rarely reported in persons younger than 30, except with exposure to bovine spongiform encephalopathy (BSE) or pituitary extract derived human growth hormone (HGH). BSE has not been found in the US.

DESIGN/METHODS: Case Reports.

RESULTS: In our hospital, 2 young men, ages 26 and 28, who were unknown to each other and had lived their entire lives in Michigan, developed rapidly progressive dementia and were simultaneously evaluated. Neither had traveled to countries with known BSE, received HGH, eaten venison or elk, or had a family history of dementia. The first patient had a 2-month history of progressive aphasia, social withdrawal, and memory difficulties. An EEG performed on admission revealed waxing and waning rhythmic spike and wave discharges. He was treated for nonconvulsive status epilepticus, which became convulsive during his hospital course. His seizures were refractory to medical therapy despite multiple anticonvulsants, including midazolam coma. His EEG became more periodic and he never recovered responsiveness even as medication was tapered. A brain biopsy and subsequent postmortem examination following his death 5 months after the onset of symptoms showed spongiform changes. The scrapie prion protein (PrPsc) was distributed in a cluster pattern as revealed by immunohistochemistry. Genetic analysis and immunoblot established that this patient had the MM2 subtype of sporadic CJD. Treatment with quinacrine had no benefit.

The second patient had a 10-month history of progressive memory loss, inappropriate behavior, violent outbursts, and difficulty performing his job. He had bradykinesia and rigidity on examination. There were no periodic discharges on EEG and CSF protein 14-3-3 was negative. Following a brain biopsy showing spongiform changes he developed startle myoclonus. The presence of PrPsc type 1 was confirmed with immunoblot and immunostaining.

Both patients had abnormal MRI scans with increased signal in the basal ganglia and cerebral cortex on T2- and diffusion-weighted images.

CONCLUSIONS: These cases expand the spectrum of sporadic CJD to include younger age of onset than previously suspected and cases presenting as non-convulsive status epilepticus. The appearance of CJD in 2 individuals within a few months of each other in southeastern Michigan may indicate that very early-onset CJD is more common than previously believed. Alternatively, other unrecognized risk factors may exist. It is important to consider CJD in young people with progressive behavioral and cognitive disturbances, even in the absence of typical EEG or CSF abnormalities.

Supported By: This study was supported by NIH grant AG14359 and grant CCU 515004 to the National Prion Disease Pathology Surveillance Center and the Michigan Alzheimers Disease Research Center (NIH grant P50-AG0871).

Kathy Stone Media Relations Manager American Academy of Neurology 1080 Montreal Avenue St. Paul, Minnesota 55116 USA ph: 651-695-2763 fax: 651-695-2791 <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000043/!x-usc:mailto:kstone@aan.com>

-- Terry J. Allen <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000043/!x-usc:mailto:tallen@igc.org>

****** [2] Date: Mon 29 Apr 2002 8:29 PM From: Terry Allen <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000043/!x-usc:mailto:tallen@igc.org> Source: USA Today 29 Apr 2002 Page 7D

Michigan brain-disease deaths 'unusual, disturbing' -

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Last fall 2 young men, ages 26 and 28, died in the same Michigan hospital of a rare brain disease that occurs mainly in elderly people. The incident, which raised fears that the human form of mad cow disease, or something similar, had emerged in the USA, prompted a swift investigation by federal health officials, but doctors familiar with the cases say there is no evidence to support that fear. They say autopsies and other tests indicate the victims died from so-called "classic" forms of Creutzfeldt-Jakob disease (CJD).

While the cases are "highly unusual and disturbing," says University of Michigan neurologist Norman Foster, the data show that the forms of CJD suffered by the young men are ones seen previously in older individuals. CJD occurs at the rate of about one person per million per year, almost always in people over age 60. What doctors feared is that a new form of CJD, possibly similar to a variant that emerged in the mid-1990s in the United Kingdom and linked to consumption of mad-cow-infected beef, had struck.

Unlike classic CJD, the new variant, vCJD, strikes mainly young adults. It has killed more than 100 people. The only known case of vCJD in the USA was diagnosed recently in a 22-year-old British woman living in Florida, who is thought to have contracted the disease in England. Mad cow disease has not been detected in cattle in the USA, but a similar disease in deer and elk is spreading in the Midwest. Chronic wasting disease (CWD) is fatal to deer and elk but is not known to cause illness in humans.

Lawrence Schoenberger of the Centers for Disease Control and Prevention in Atlanta says the agency sent investigators to Michigan in late August 2001, when the victims were still alive. "The key thing here is the 2 were right together. We were worried that there was maybe a common exposure, but our investigation revealed that was not the case." The men lived in adjacent counties but did not know each other, he says.

In the rare cases when CJD strikes before age 30, it is often caused by a hereditary form of the disease, says Foster, and "tests are continuing to see if that may be a factor in these cases." But extensive family interviews determined that neither man had a family history of dementia, nor had they eaten venison or elk meat or visited countries where mad cow disease has been detected.

"We feel as comfortable as anyone can that this is not related to either CWD or (mad cow disease)," says Foster, who treated the patients at the University of Michigan Medical Center in Ann Arbor. Not everyone is comfortable. "I discount the statement that these 2 young people, dying at the same time in the same hospital in southeast Michigan, did not eat venison, after living their entire lives in that state," says John Stauber of the Center for Media & Democracy and co-author of Mad Cow USA.

He suspects a new American variant of CJD, perhaps related to chronic wasting disease, may be emerging. "Any attempt to portray these CJD deaths as some sort of 'normal' occurrence that has simply, to date, gone unobserved is absurd," Stauber says. Current estimates of only 5 cases per billion of CJD in people 30 and younger may be incorrect, says Foster, who co-wrote a report on the cases presented this month at a meeting of the American Academy of Neurology.

"The fact that they both occurred at the same time in a relatively small population suggests that (CJD in younger people) may be more common than previously suspected," Foster says. Doctors don't expect to see it in young people, so misdiagnosis may occur. " Any young individual with progressive neurologic disease should be considered for CJD."

He says the cases also underscore the need for a national system to seek out and report all cases of CJD. "There certainly is the possibility that other cases have been seen and not diagnosed, or even if diagnosed, not reported."

[Byline: Anita Manning]

-- Terry j allen <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000043/!x-usc:mailto:tallen@igc.org>

[At present a link between CWD and CJD in the USA or Canada has not been established. Unfortunately, reviewing the UK and European experience, it would not be a surprise if such a link were identified. Clearly we are very early in our understanding of prion disease and early in our identification of the full range and spectrum of the prion disease presently manifested as CWD in cervids in North America. The occurrence of 2 cases of sporadic CJD in unrelated individuals below the age of 30 is unusual and warrants the scrutiny it has been receiving. We await more information as it becomes available.

Some useful reference for our readers:

1: Belay ED, Gambetti P, Schonberger LB, Parchi P, Lyon DR, Capellari S, McQuiston JH, Bradley K, Dowdle G, Crutcher JM, Nichols CR. Creutzfeldt-Jakob disease in unusually young patients who consumed venison. Arch Neurol. 2001 Oct;58(10):1673-8.

2. Brown P, Will RG, Bradley R, Asher DM, Detwiler L. Perspective: Bovine Spongiform Encephalopathy and Variant Creutzfeldt-Jakob Disease: Background, Evolution, and Current Concerns. EID 7(1) Jan-Feb 2001 <http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm>

3. Holman RC, Khan AS, Belay ED, Schonberger LB. Dispatches: Creutzfeldt-Jakob Disease in the United States, 1979-1994: Using National Mortality Data to Assess the Possible Occurrence of Variant Cases. EID 2(4) Oct-Dec 1996 <http://www.cdc.gov/ncidod/eid/vol2no4/holman2.htm>

4. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Research letter: Creutzfeldt-Jakob Disease in the United States: 1979-1998. JAMA 284(18) 8 Nov 2000 <http://jama.ama-assn.org/issues/v284n18/ffull/jlt1108-6.html>

5. Surveillance for Creutzfeldt-Jakob Disease. MMWR, 45(31):665-668 9 Aug 1996 <http://www.cdc.gov/mmwr/preview/mmwrhtml/00043220.htm> - Mod.MPP] ..................................lm/mpp/pg/lm

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http://www.promedmail.org/pls/otn/f?p=2400:1202:218493::NO::F2400_P1202_CHECK_DISPLAY,F2400_P1202_PUB_MAIL_ID:X,18062



Monday, July 27, 2009



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

WHY DID THIS VIDEO NOT SHOW ON EVERY NEWS CHANNEL IN THE U.S.A. $$$

IT IS A DAMNING VIDEO !!!

I WATCHED THIS RECENTLY, and had never seen it. i was so mad, i was spitting nails out faster than a framing gun.

WHY DID THE CANADIAN MEDIA ONLY PRESENT THIS TO THE U.S.A. PUBLIC (thank you very much though), and why has the U.S.A. MEDIA FAILED US ???

WHY DID R-CALF NOT SHOW THIS ??? where was r-calf when you needed them back then $$$

SNIP...

Monday, July 27, 2009

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



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




Tuesday, July 14, 2009

U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST

WHERE did we go wrong $$$




http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html




Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]




http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html




Transmissible mink encephalopathy - review of the etiology




http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.html




Wednesday, July 1, 2009

Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)




http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html




Monday, June 01, 2009 Biochemical typing of pathological prion protein in aging cattle with BSE

SOMETHING TO PONDER ???

O.K. confusious asks, IF all these new atypical BSEs i.e. new strains of mad cow disease is just an 'OLD COW PRION DISEASE', why then can not the 'old human prion disease' such as the sporadic CJD, be from an 'old cow prion disease', same as the nvCJD 'young people mad cow disease' (which also happens in 74 year old), but why cannot the 'old cow prion diseases', i.e. l-BSE, h-BSE, and ibncBSE, cause the 'old people prion disease', which looks like sporadic CJD. seems that is what some of the pathology is showing ???

OH, that probably makes too much sense, and that the only answer could be that it's all just a happenstance of bad luck and or a spontaneous event, that just happens out of the clear blue sky $$$

IF this is the case, then where are all the SPONTANEOUS BSE CASES OF MAD COW DISEASE IN THE U.S.A., AND WHERE HAVE THEY BEEN BURIED IN THE USA OVER THE LAST 25 YEARS ???




http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html




TSS

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

(strange, this would have been my mothers birthday, but she had been dead for 8 years hvCJD confirmed here in the U.S.A....TSS)

CBC’s The National

October 17, 2005

Safe To Eat?

PETER MANSBRIDGE (HOST):

Safe To Eat? She thought her son died of a random illness, one with no known cause, no cure. Now some scientists are questioning whether there's a new link to mad cow disease. Kelly Crowe reports. -

For years, scientists have known that B.S.E. causes variant Creutzfeldt-Jakob disease. What some people call the human form of Mad Cow Disease. But another form of C.J.D., Sporadic C.J.D., has always confounded them. The most common theory has been that the deadly illness occurs spontaneously with no known cause. Now some of the world's leading scientists in the field are having another look at sporadic C.J.D. and the possibility that it too is linked to mad cow. Here's Kelly Crowe with a feature report.

KELLY CROWE (REPORTER):

It starts out slowly. At first, the victims don't know what's wrong with them. They can't put their finger on it. They keep making little mistakes. The spelling mistakes that just look sloppy... numbers become easily confused... the words on the page become blurry. It's the beginning of a terrifying slide in to dementia and death. That's what happened to Jeff Schwan. Little by little, his brain was ravaged by a disease so rare, his mother had never even heard of it.

UNIDENTIFIED WOMAN (MOTHER OF JEFF SCHWAN):

And finally on August 11th, we received words you'll never want to hear. He has a disease that has no treatment and no cure, and we just tried to take that in.

NORMAN FOSTER (DOCTOR):

Check eye movements, look right here at my finger.

KELLY CROWE (REPORTER):

It was Dr. Norman Foster who discovered the terrible truth. He specializes in diseases of the brain, and he's the one who finally figured out what was wrong with Jeff Schwan.

NORMAN FOSTER (DOCTOR):

The major problem was a seizure disorder, and that was investigated and treated, but despite treatment, he became progressively worse. And it was unclear at the time what was causing these seizures, and it was suspected that this was due to an encephalitis or meningitis or some other problem, and I strongly advocated that everything be done to identify what the cause of this is, and that led to a brain biopsy. When we examined the tissue under the microscope, we were somewhat surprised to find evidence of Creutzfeldt-Jakob disease.

KELLY CROWE (REPORTER):

Jeff Schwan died from a mysterious illness called Sporadic Creutzfeldt-Jakob disease or Sporadic C.J.D. It's a rare and fatal brain-wasting disease that seems to strike out of nowhere. But was it really just bad luck that killed this healthy 26-year-old man, or is there another explanation? Sporadic Creutzfeldt-Jakob disease is a type of prion disease. Prions are proteins found in humans and other mammals, but when an altered form of the prion appears, it somehow starts a critical chain reaction turning healthy prions in to deadly ones that ultimately destroy the brain. Prion diseases are always fatal. There is no cure, no treatment. And science now knows that prion diseases can be spread by eating meat. It was first realized here in Papua New Guinea back in 1957 where a brain-wasting disease called Curu was sweeping through a tribe of cannibals.

Scientists realized these people were developing Curu after feasting on the remains of their dead who were already infected. It was the first evidence that prion diseases could be spread through eating infected material. 30 years later, British cattle began developing a prion disease. It was called B.S.E. or Mad Cow Disease. It was spread when the animals ate feed made from diseased cattle. Then young Britons began dying, and scientists realized humans could catch a prion disease from eating infected beef. That disease is called Variant C.J.D. So far, it has claimed 170 victims. But none of that seems to explain what happened to Jeff Schwan. He had the other prion disease, the one that is thought to strike at random, so-called Sporadic C.J.D. Like the other prion diseases, the brain fills with sponge-like holes, but scientists don't know what causes sporadic C.J.D., and some are asking, could it also be caused by eating meat? Here's one possible clue: The disease sometimes shows up in clusters in people who live near each other. It happens too often to be explained only by chance. British epidemiologist Simon Cousins worked on two scientific studies that documented clusters of the disease in both England and France. The studies concluded that it must be caused by something on the outside, that it can't be just a spontaneous disease.

SIMON COUSINS (EPIDEMIOLOGIST):

The spontaneous event would be, doesn't really explain why they might be clustering. So the clustering is pointing one in the direction of thinking from time to time people are exposed to a common external source.

KELLY CROWE (REPORTER):

One common external source, infected meat. It's a frightening possibility that is being actively investigated by some European scientists. Here in Switzerland, there was an epidemic of Mad Cow Disease in the 1990s, and now they're seeing a more than doubling in the rate of Sporadic C.J.D. Swiss scientists think there might be a connection.

ADRIANO AGUTZY (SCIENTIST):

What we need to find out is whether the whole problem of the enhanced Creutzfeldt-Jakob does, indeed, have something to do with mad cow's disease, but we certainly did have our definite window of exposure, and so if we now, if we had B.S.E. ten years ago and now we have enhanced Creutzfeldt-Jakob disease, it's unavoidable to ask the question whether the two phenomena are related.

KELLY CROWE (REPORTER):

DR. Adriano Agutzy is one of the world's experts on prion diseases. He says he has ruled out most of the other explanations, and now his main working hypothesis is that at least some Sporadic C.J.D. in Switzerland could be another form of human Mad Cow Disease.

ADRIANO AGUTZY (SCIENTIST):

But this by no means excludes that B.S.E. may manifest itself in humans with different characteristics, and maybe B.S.E. in Switzerland is also different from B.S.E. in the U.K., and then variant C.J.D. will also be different. So I think from the U.K. experience, it's impossible to draw the conclusion that B.S.E. will only give rise to what we know as variant C.J.D.

KELLY CROWE (REPORTER):

What it means is cattle infected with prion disease might be causing Sporadic C.J.D. To find out, the scientists are trying to match the tissue from infected Swiss cattle with the tissue from Swiss victims. If the tissue looks the same on the lab tests, then it will be strong evidence the two are connected. Right next door in Italy, they might have already made that connection. This doctor was studying the brains from B.S.E. infected cattle when he noticed a form of the disease he'd never seen before. He realized it was a new form of Mad Cow Disease. It was the first time scientists realized there could be more than one kind of prion disease in cattle.

UNIDENTIFIED MAN:

So our assumption is that since there is this biochemical similarities together with this, we think there might be a connection between the two.

KELLY CROWE (REPORTER):

He got a second shock when he ran the new cattle prion through the lab tests. It looked exactly like Sporadic C.J.D. He could hardly believe his eyes. He was looking at possible proof that humans could catch a second prion disease from cattle.

UNIDENTIFIED MAN:

Yes, this is only a biochemical evidence because at the beginning when B.S.E. has been discovered and the Variant C.J.D. had been discovered in the U.K., They found the single cell. I mean, the biochemical part of both B.S.E. and variant were similar. We found the same biochemical. There are pathological similarities and ecological similarities.

KELLY CROWE (REPORTER):

There is still one more step to prove the link. This new strain of B.S.E. will be injected into mice that have human genes. It will take two years, but the results will bring scientists a little bit closer to the answer of whether Sporadic C.J.D. is caused by meat. ADRIANO AGUTZY (SCIENTIST):

I think that that is a possibility. Personally, I would say that it's possible that some of the cases are caused, I mean, maybe what would cause Sporadic C.J.D. is a collection of different diseases, and some of it could actually be transmission of B.S.E.

UNIDENTIFIED MAN:

It might be a possibility because it is an infectious disease. I mean, if you get a piece of brain of this with classic C.J.D. and you inoculate the animal, you transmit the disease, but on the other side, it's not clear whether the animal transmit the disease to man.

KELLY CROWE (REPORTER):

Scientists agree that cattle prion disease must be kept out of the human food supply. The problem is finding it before the animal is slaughtered. Bitter experience has already proven that the disease can be lurking even as officials boast that their herd is B.S.E.-free. After years of making those claims, the U.S. has had to admit to a homegrown case of B.S.E. in a Texas cow this past June. And that case was discovered only after testing was dramatically increased. And yet the U.S. and Canada are still only testing cattle that look sick. And with that kind of testing and millions of animals slaughtered every year, the disease is easy to miss. A lesson the Italians already learned. In Italy, they didn't know for sure that they had Mad Cow Disease until they started testing, not just the animals that looked sick, but every single animal over 24 months that goes into the food chain. Now four years later, they've only had one animal that looks sick, but they've found more than 130 cases of Mad Cow Disease in healthy looking animals. In other words, if they hadn't been testing those 130 animals would have gone into the food chain. In North America, they're only looking at symptomatic cases, zero so they could be missing a lot of disease.

UNIDENTIFIED MAN:

Sure, they take only neurological cattle, cattle with neurological symptoms or downer cattle. So this is the so-called passive surveillance. When you have neurological, you make the potential diagnosis of C.J.D. And the only way to get rid of this is that all the animals should be tested, and people at least buy a piece of meat to say this is B.S.E.-free.

KELLY CROWE (REPORTER):

Dr. Agutzy says the United States isn't trying hard enough to find prion disease in its cattle.

ADRIANO AGUTZY (SCIENTIST):

I think that in North America, there is a huge problem because North America has refused for many years to put in place any kind of serious surveillance of cattle, and I think this is a disgrace, and it really cries to Heaven about the fact that particularly the U.S. has just refused to even take into consideration the possibility that B.S.E. may be prevalent. It's a huge problem.

KELLY CROWE (REPORTER):

It's also not clear how widespread Sporadic C.J.D. is. The final diagnosis can only be made after death by examining the brain in an autopsy, but today autopsies are rarely done. And although Sporadic C.J.D. is a rare condition, estimated at one in a million, Dr. Norman Foster suspects the rate is higher.

NORMAN FOSTER (DOCTOR):

In many states in the United States, if a physician suspects a case, they can report it as a public health problem, but there's no mechanism to investigate or no way to pursue this in a systematic way.

KELLY CROWE (REPORTER):

So you could be missing lots of cases?

NORMAN FOSTER (DOCTOR):

So we are missing lots of cases.

KELLY CROWE (REPORTER):

Jeff Schwan is on the official record as just another unfortunate victim of a rare disease that seems to strike for no reason. And for his mother, it is the unanswered questions that weigh most heavily on her shoulders.

UNIDENTIFIED WOMAN (MOTHER OF JEFF SCHWAN):

So all of these people who are dying of Sporadic C.J.D., they don't have an answer for. It's very, very frustrating because we want answers.

KELLY CROWE (REPORTER):

To get those answers, she must wait for the slow deliberate pace of science. Kelly Crowe, CBC News, Sterling Heights, Michigan.



http://www.healthcoalition.ca/cbccjd.pdf




P.S.S. (July 31, 2009)



PLEASE REMEMBER, (and i had to wrote to terry schwann to make sure my mind was not decieving me, and she did confirm it was NOT), that there was another young man, 28 years old, in the same hospital, the same week as jeff schwann 26 was, that he too had cjd.



>>>There was another young man, 28, diagnosed with CJD as well. Same floor, same week. He died in Feb. 2002 I think. This young man's aunt contacted me some time later and confirmed CJD, but the young man's wife really did not want any contact or discussion--SNIP...TSS...He was in the military and had been stationed in Europe...and I never heard the final diagnosis...but I can guess...sCJD. They lived in the Port Huron area (Michigan). Dr. Norman Foster (in the video) diagnosed him as well. I believe he's now practicing in Utah.<<<


TSS



WHY DID THIS VIDEO NOT SHOW ON EVERY NEWS CHANNEL IN THE U.S.A. $$$


IT IS A DAMNING VIDEO !!!


I WATCHED THIS RECENTLY, and had never seen it. i was so mad, i was spitting nails out faster than a framing gun.


WHY DID THE CANADIAN MEDIA ONLY PRESENT THIS TO THE U.S.A. PUBLIC (thank you very much though), and why has the U.S.A. MEDIA FAILED US ???


WHY DID R-CALF NOT SHOW THIS ??? where was r-calf when you needed them back then $$$


Thursday, April 9, 2009

Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed



http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html



http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html#comments



Sunday, April 12, 2009 r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada



http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html



http://prionunitusaupdate2008.blogspot.com/2009/04/cjd-foundation-sides-with-r-calfers-no.html#comments



Tuesday, July 14, 2009

U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST



WHERE did we go wrong $$$



http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html



Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]



http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html



Transmissible mink encephalopathy - review of the etiology



http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.html



Wednesday, July 1, 2009

Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)



http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html



Monday, June 01, 2009 Biochemical typing of pathological prion protein in aging cattle with BSE

SOMETHING TO PONDER ???

O.K. confusious asks, IF all these new atypical BSEs i.e. new strains of mad cow disease is just an 'OLD COW PRION DISEASE', why then can not the 'old human prion disease' such as the sporadic CJD, be from an 'old cow prion disease', same as the nvCJD 'young people mad cow disease' (which also happens in 74 year old), but why cannot the 'old cow prion diseases', i.e. l-BSE, h-BSE, and ibncBSE, cause the 'old people prion disease', which looks like sporadic CJD. seems that is what some of the pathology is showing ???

OH, that probably makes too much sense, and that the only answer could be that it's all just a happenstance of bad luck and or a spontaneous event, that just happens out of the clear blue sky $$$

IF this is the case, then where are all the SPONTANEOUS BSE CASES OF MAD COW DISEASE IN THE U.S.A., AND WHERE HAVE THEY BEEN BURIED IN THE USA OVER THE LAST 25 YEARS ???



http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html



USDA FDA CERTIFIED MAD COW FEED BAN of August 4, 1997, i.e. BSE FIREWALLS, never existed, it was nothing more than ink on paper ;

10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

___________________________________

PRODUCT

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.

REASON

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI

___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html

NEW URL



http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm



Thursday, March 19, 2009 MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$



http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.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



U.S.A. PLAYING A SERIOUS GAME OF 'PASS IT FORWARD' WITH T.S.E.'s ...TSS



Friday, July 24, 2009

UW Hospital and Clinics Addresses Creutzfeldt-Jakob Disease Risk



http://creutzfeldt-jakob-disease.blogspot.com/2009/07/uw-hospital-and-clinics-addresses.html




Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

6 acquitted in French trial over hormone deaths

6 acquitted in French trial over hormone deaths
14 Jan 2009, 1858 hrs IST, AP


PARIS: A French court acquitted six people on Wednesday over the deaths of at least 114 people who contracted a brain-destroying disease after being treated with tainted human growth hormones.

The verdict followed a 16-year investigation into the deaths from Creutzfeldt-Jakob disease, or CJD.

The Paris court acquitted the six doctors and pharmacists of manslaughter and other charges in the verdict Wednesday.

The case stemmed from a 20-year program that involved collecting hormones from the pituitary glands of human corpses to treat thousands of French children who suffered from a deficiency in the secretion of growth hormone.

The cases were not of the widely known ``Mad Cow'' variant of CJD.

The programme ended in 1988.




http://timesofindia.indiatimes.com/World/6_acquitted_in_French_trial_over_hormone_deaths/articleshow/3979075.cms#write




>>> The cases were not of the widely known ``Mad Cow'' variant of CJD.<<<


homicide is homicide, period. whether or not you eat a burger with a TSE i.e. prions, or whether someone harvest some organs in a manner of which diseased organs were given out i.e. 'the body snatchers'. BOTH those industries KNEW of the risk from there tainted products, rules were in place, and they were broken, people died, and are still dying. being stupid, incompetent, and or greedy cannot be an excuse anymore. ...


Saturday, January 26, 2008

CJD HGH BODY SNATCHERS


http://creutzfeldt-jakob-disease.blogspot.com/2008/01/cjd-hgh-body-snatchers.html



http://creutzfeldt-jakob-disease.blogspot.com/2008/07/creutzfeldt-jakob-disease-in-recipients.html



Cadaver corneal transplants -- without family permission...



http://www.mad-cow.org/~tom/dec99_news.html#bbb



The documents below were provided by Terry S. Singeltary Sr on 8 May 2000. They are optically character read (scanned into computer) and so may contain typos and unreadable parts. TIP740203/l 0424 CONFIDENTIAL


http://www.mad-cow.org/00/may00_news.html#aaa


http://www.whale.to/v/singeltary7.html



http://www.whale.to/v/singeltary.html




(Not to forget about the potential for some BSE cases to come from vaccinations containing pituitary-derived SRMs.)

TWA LITTLE minute


http://www.bseinquiry.gov.uk/files/yb/1988/06/10001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1988/06/13010001.pdf



http://www.bseinquiry.gov.uk/files/yb/1988/06/14006001.pdf



COMMERCIAL IN CONFIDENCE


http://www.bseinquiry.gov.uk/files/yb/1988/09/06005001.pdf



http://www.bseinquiry.gov.uk/files/yb/1988/10/06005001.pdf



NOT FOR PUBLICATION


http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf



http://www.bseinquiry.gov.uk/yb/1988/11/04003001.pdf



http://www.bseinquiry.gov.uk/files/yb/1988/04/00007001.pdf



http://www.bseinquiry.gov.uk/files/yb/1988/07/00007001.pdf



http://www.bseinquiry.gov.uk/files/yb/1988/09/00004001.pdf



http://www.bseinquiry.gov.uk/files/yb/1988/10/00003001.pdf



http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1989/01/26007001.pdf



http://www.bseinquiry.gov.uk/files/yb/1989/01/30001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf



NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE snip... I was quite prepared to believe in unofficial pituitary hormones, also in the 1970's, whether as described by Dr. Little, or in other circumstances, for animal use. snip... The fact that there were jars of pituitaries (or extract) around on shelves is attested by the still potent 1943 pituitaries, described in Stockell Hartree et al. (J/RF/17/291) which had come from the lab. at Mill Hill. Having taken the trouble to collect them, they were not lightly thrown out...



http://www.bseinquiry.gov.uk/files/ws/s467bx.pdf



more on the 1968 medicine act, they forgot to follow



http://www.bseinquiry.gov.uk/files/yb/1989/01/30008001.pdf



Draft cover letter to product licence holders (considered by Human and Vet Medicines including deer)



http://www.bseinquiry.gov.uk/files/yb/1989/02/22008001.pdf



http://www.bseinquiry.gov.uk/files/yb/1989/02/22011001.pdf



(It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control.)



http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf



http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf



http://www.bseinquiry.gov.uk/files/yb/1988/06/07010001.pdf



TWA LITTLE STATEMENT 331



http://www.bseinquiry.gov.uk/files/ws/s331.pdf




Sunday, May 18, 2008

MAD COW DISEASE BSE CJD CHILDREN VACCINESTIP740203/l 0424 CONFIDENTIAL


http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html


Monday, May 19, 2008

SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS


http://bseinquiry.blogspot.com/2008/05/sporadic-cjd-in-farmers-farmers-wives.html


Sunday, May 18, 2008


BSE, CJD, and Baby foods (the great debate 1999 to 2005)


http://bseinquiry.blogspot.com/2008/05/bse-cjd-and-baby-foods-great-debate.html


BSE Inquiry DRAFT FACTUAL ACCOUNTS

DFA's


http://bseinquiry.blogspot.com/2008/05/bse-inquiry-draft-factual-account-dfa.html



Sunday, December 28, 2008

MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy



http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html




http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&d=APHIS-2006-0041-0006





From: Terry S. Singeltary Sr.

To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000004/!x-usc:mailto:FREAS@CBER.FDA.GOV

Cc: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000004/!x-usc:mailto:william.freas@fda.hhs.gov ; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000004/!x-usc:mailto:rosanna.harvey@fda.hhs.gov

Sent: Friday, December 01, 2006 2:59 PM

Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION

snip...

ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)

THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.

These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

snip... 48 pages...



http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8




Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Docket Type Rulemaking Document APHIS-2007-0033-0001 Document Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Public Submission APHIS-2007-0033-0002.1 Public Submission Title Attachment to Singeltary comment



http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=090000648027c28e



Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2007.



http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf




http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html




Thursday, November 27, 2008

Prion diseases are efficiently transmitted by blood transfusion in sheep
TRANSFUSION MEDICINE



http://vcjdblood.blogspot.com/2008/11/prion-diseases-are-efficiently.html



Wednesday, December 10, 2008



Evaluation of FSIS Management Controls Over Pre-Slaughter Activities (Audit Report 24601-7-KC)



Executive Summary

USDA CERTIFIED DEAD STOCK DOWNER COW SCHOOL LUNCH PROGRAM



http://downercattle.blogspot.com/





stupid is, as stupid does, (forest gump)

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

Mum Christine Lord wants justice after CJD cover up

Mum wants justice after CJD cover up

Campaigner whose son died of human form of mad cow disease to lobby MLAs

By Joe Oliver Sunday, 11 January 2009

CJD victim Jonathan Simms and his father Don.

A campaigning mum is set to visit Northern Ireland in her quest for justice after the devastating death of her son from the human form of ‘mad cow’ disease.

Freelance journalist Christine Lord is planning to address members of the Assembly and family groups — as fears grow over a new wave of the killer brain bug.

She also hopes to set up a private meeting with the family of west Belfast man Jonathan Simms — the world’s longest-known survivor of variant Creutzfeldt-Jakob Disease (vCJD).

At 24, Jonathan is the same age as her son Andrew who died just over a year ago.

Since then — and following Andrew’s dying request — Christine has campaigned relentlessly to expose the key players behind the BSE scandal and the horror of vCJD.

Christine, from Southsea, Hants, recently petitioned Prime Minister Gordon Brown in Downing Street to release confidential documents about Government policy regarding BSE.

She told Sunday Life: “The cover up has gone on too long — it’s time we had justice. My beautiful, gentle boy was reduced to a shell. He had a terrible and distressing death.

“He was blind, deaf, quadriplegic and unable to recognise or remember anything or anyone. If the Government and senior officials had not ignored evidence and withheld crucial information, then all the victims of vCJD, including my son, would still be alive.”

Christine has already been in touch with former first minister Ian Paisley and was overwhelmed by the letters of support she received from Northern Ireland since telling her harrowing story in a BBC documentary.

“I wrote to Dr Paisley because I was aware that one of the victims of vCJD in Northern Ireland was a member of his party,” she said.

Andrew Hunter, who was just 27, was a DUP member of Newtownabbey Borough Council and died from the disease at his home in Rathcoole in April 2002.

The first person from the province to contract vCJD was 30-year-old Maurice Callaghan from west Belfast. He died in 1995, leaving a wife who was pregnant with their second child, and a daughter.

The first wave of vCJD, caused by eating infected beef products in the 1980s and early 1990s, has been responsible for 164 deaths.

All victims belonged to a gene type known as MM. Clinical tests suggest that new sufferers have an MV gene type, although this cannot be confirmed until a brain biopsy is carried out after death.

But the possibility has raised concerns that the illness may have a longer incubation period.

Christine does not know how Andrew contracted vCJD, but revealed that she stopped giving her children meat when the first fears where raised.

She believes he may have been carrying it in his system before 1994, although he showed no symptoms until the end of 2006 when he was initially told he was “depressed”.

Her daughter Emma (18) has shown no sign of infection.

“The disease affects predominantly young people in their teens and twenties,” she said.

“Its agent, BSE, was given free rein again and again to enter the food chain, wreck lives, families, careers, homes and futures. There was a wealth of scientific knowledge that BSE was harmful to humans, but they still allowed the most toxic materials into the food chain to be ingested by infants and children.

“They did nothing to stop the threat to school meals, baby food and the infected serum in childhood immunisations.”

Christine decided against giving her son pentosan polysulphate — the blood-thinning and anti-inflammatory therapy previously only tested on animals.

“I know the Simms family in Belfast had to fight a battle in the courts to get it for their son and I am genuinely delighted to hear the consensus that he is no longer terminally ill,” she said.

“But it was something I discussed with my son and one of the reasons I would very much like to meet the Simms family.

“When I’m in Northern Ireland I want to meet the political parties across the whole spectrum and, of course, I want support for my petition which already has thousands of signatures.”

She added: “My son’s death was totally avoidable.

“Those in the Conservative government at the time and their advisors knew at the earliest stages that BSE had severe implications for human life.

“They held the smoking gun that killed my son and many others. I want them publicly and legally held accountable.

“That way I can finally win justice for Andrew and all victims of vCJD past, present and, tragically, those still to come.”

The Government’s chief adviser on vCJD warned recently there could be a second wave of deaths over the coming years involving anything between 50 and 350 people.

l To visit Christine’s website click onto www.justiceforandy.com

http://www.belfasttelegraph.co.uk/sunday-life/mum-wants-justice-after-cjd-cover-up-14136640.html


JUSTICE FOR ALL TSE VICTIMS !!!

Greetings to ALL human CJD/TSE victims and to their families,

THERE is more to this story than the UKBSEnvCJD adolescents only theory of CJD, and the rest i.e. 85%+ are just a happenstance of bad luck, or simply a flipped out protein. while i applaud Christine Lord's campaign to expose the key players behind the BSE scandal and the horror of vCJD, sadly, we are only speaking of a very small part, of a much larger global problem with human and animal TSEs, and by ignoring these other TSEs, you are only allowing this agent to spread through a multitude of proven routes and sources. Some of us have been fighting for over a decade to expose a much larger global cover-up of all strains of human and animal TSE, especially, the sporadic CJD's. sporadic CJD is not a single strain, but a multitude of many yet unknown strains, another of which was discovered (or announced) last year in 2008 here in the USA.

IT'S called STRAINS !

Sunday, December 28, 2008

MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy

8 YEARS IN REVIEW OF THE MAD COW DEBACLE IN THE USA ;

http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html


Tuesday, January 06, 2009

CWD Update 93 December 29, 2008

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-update-93-december-29-2008.html


Monday, December 1, 2008 When Atypical Scrapie cross species barriers

http://nor-98.blogspot.com/2008/12/when-atypical-scrapie-cross-species.html


USA PRION UNIT BLOG

http://prionunitusaupdate2008.blogspot.com/


Sunday, April 20, 2008 Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008

Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.

see full text ;

http://prionunitusaupdate2008.blogspot.com/2008/04/progress-report-from-national-prion.html


Friday, December 12, 2008

The prion strain phenomenon: Molecular basis and unprecedented features

http://bse-atypical.blogspot.com/2008/12/prion-strain-phenomenon-molecular-basis.html


Wednesday, December 10, 2008

Evaluation of FSIS Management Controls Over Pre-Slaughter Activities (Audit Report 24601-7-KC) USDA CERTIFIED DEADSTOCK DOWNER COW SCHOOL LUNCH PROGRAM

http://downercattle.blogspot.com/2008/12/evaluation-of-fsis-management-controls.html


Wednesday, August 20, 2008 Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?

http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html


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


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://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html


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


sporadic Fatal Familial Insomnia

http://sporadicffi.blogspot.com/


THE PATHOLOGICAL PROTEIN

Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam

CHAPTER 14 LAYING ODDS

Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.

http://www.thepathologicalprotein.com/


The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003

doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI

Tracking spongiform encephalopathies in North America

Original TextXavier Bosch

"My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem."

49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realized that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.

Singeltary was greatly demoralized at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.

Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.

To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.

Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticized for not having performed enough prionic tests in farm deer and elk.

Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.

Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.

Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modeled on that established in the UK, he points out.

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.

CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.

Greetings,

he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.<<<

actually, that quote was from a more recent article in the Journal of Neurology (see below), not the JAMA article. ...TSS

http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(03)00715-1/fulltext


http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/%20fulltext


http://www.ncbi.nlm.nih.gov/pubmed/12906010


http://infection.thelancet.com/journal/journal.isa


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


Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

Terry S. Singeltary, Sr Bacliff, Tex

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT

http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT


http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT


2 January 2000 British Medical Journal U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

http://www.bmj.com/cgi/eletters/320/7226/8/b#6117


15 November 1999 British Medical Journal vCJD in the USA * BSE in U.S.

http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406


Creutzfeldt Jakob Disease

http://creutzfeldt-jakob-disease.blogspot.com/


CJD TEXAS (cjd clusters)

http://cjdtexas.blogspot.com/


USA WRITTEN CJD QUESTIONNAIRE ???

http://cjdquestionnaire.blogspot.com/


The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

http://www.cjdfoundation.org/fact.html


Attending Dr.: Date / Time Admitted : 12/14/97 1228

UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report

FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858

FINAL AUTOPSY DIAGNOSIS

I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.

http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html


Friday, December 12, 2008

Creutzfeldt-Jakob disease (CJD) update report Emerging Infections/CJD Published on: 12 December 2008

http://creutzfeldt-jakob-disease.blogspot.com/2008/12/creutzfeldt-jakob-disease-cjd-update.html


HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf


Sunday, May 18, 2008

MAD COW DISEASE BSE CJD CHILDREN VACCINES

TIP740203/l 0424 CONFIDENTIAL

http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html


Monday, May 19, 2008 SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS

http://bseinquiry.blogspot.com/2008/05/sporadic-cjd-in-farmers-farmers-wives.html


Sunday, May 18, 2008 BSE, CJD, and Baby foods (the great debate 1999 to 2005)

http://bseinquiry.blogspot.com/2008/05/bse-cjd-and-baby-foods-great-debate.html


BSE Inquiry DRAFT FACTUAL ACCOUNTS DFA's

http://bseinquiry.blogspot.com/2008/05/bse-inquiry-draft-factual-account-dfa.html



Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518