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From: TSS ()
Subject: Re: Rare Brain Disease Could Be to Blame for Three Northeast Indiana Deaths
Date: May 21, 2007 at 2:36 pm PST

In Reply to: Re: Rare Brain Disease Could Be to Blame for Three Northeast Indiana Deaths posted by TSS on May 19, 2007 at 7:43 am:

Brain Disease Update: Interview with State Health Dept.

May 21, 2007 03:56 PM CDT


(WANE -- Indianapolis) -- It's called CJD or Creutzfeldt-Jakob disease. There are only a few ways to get it: at random, from genetics, and the least likely, you can get the variant form by eating mad cow infested meat.

Last week we told you about three reports of this brain disease in Northeastern Indiana. The Center for Disease Control says only one-in a million people get it. We wanted to know why so many cases were popping up in our area, so we went to the state health department.

But because the state doesn't consider CJD a reportable disease, there's no way of confirming how many cases happen in Indiana or any specific area within the state. An autopsy is required to figure that out. The people in charge of tracking this at the state level told us they don't track it because there's nothing they can do about it.

"Usually whatever diseases we're talking about we give specific ways to avoid it." state epidemiologist Bob Teclaw said. "For CJD there's really nothing we have no idea."

More than 60 percent of states do track Creutzdeldt-Jakob disease so they can look for anomalies in that one-in a million statistic.

http://www.wane.com/Global/story.asp?S=6547242&nav=0RYb


----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Monday, May 21, 2007 1:55 PM
Subject: Creutzfeldt Jakob Disease and Human and Animal TSE in the USA


> Greetings Dr. McMahan,
>
>
> Hello, my name is Terry S. Singeltary Sr., and I was sadden to hear of the
> recent 3 cases of CJD in such a short time span in your area. There are many
> factors that could play into this, and the article I read in the recent
> paper had several errors in it.
>
>
> A NewsChannel 15 Exclusive
> Rare Brain Disease Could Be to Blame for Three Northeast Indiana Deaths
>
>
> snip...
>
>
> vCJD cases have also occurred when people had surgery and surgical
> instruments were contaminated. Now sterilization procedures prevent that
> from happening.
>
> ???????????????????????????????????????
>
> wrong ! vCJD has never been _documented_ to transmit via the surgical arena.
> now that does not mean it has not happened. IT HAS happened with the
> sporadic CJDs now documented at 6 different phenotypes, my mothers was the
> Heidenhain Variant of CJD i.e. hvCJD. however, there are now 4 cases of
> transfusion related nvCJD that have been documented. and the statement that
> sterilization prevents cjd from happening is wrong. there are sterilization
> procedures that reduce the infectivity, but does not remove it all together,
> and most medical facilities do not use the most up to date sterilization
> procedures that would kill a TSE in totality, that I am aware of to date.
> ...TSS
>
>
> A third way vCJD was contracted was through a growth hormone made from the
> pituitary glands of cadavers. The mutated prion can't be killed with
> traditional disinfection procedures, so they were carried into the hormone
> pills. Now the hormone supplements are made artificially, so there is no
> chance of contamination.
>
>
> ???????????????????????????????????????
>
> wrong again, this has only been documented to have happened from sporadic
> CJD. and they are still putting specified risk materials i.e. SRMs in
> nutritional supplements for humans and animals, they also have human growth
> hormones. for instance Armour Thyroid is made from an extract of pig
> thyroid, and use to be made from the bovine thyroid. but that's another
> story. ...TSS
>
>
> Dr. McMahan,
>
> I wish to send you the following data for your own personal use. I do not
> even expect a reply. I am what they call politically incorrect on this
> issue, very biased, but I can assure you that mad cow BSE and BASE has been
> in the USA for decades undetected. the USA has the most documented animal
> TSEs in species than any other country, and most all has been rendered and
> fed back to animals for human and animal consumption. but the sporadic and
> spontaneous, UKBSEnvCJD only theory is totally bogus, including the
> diagnostic criteria. it changed when Vickey Rimmer died at 16 in the UK. The
> elderly are expendible, but the kids and the dogs and cats are not. I hope
> you take the time to read this. You are only aware of one side of this. I
> have wasted 10 years daily sitting here trying to .............well, im
> rambling now, please read the latest science.
>
>
> P.S. if you speak with anyone at CWRU or the CJD Foundation ''INC'', you
> will probably find that I am not well liked there. but that is neither here
> nor there, it's the science and that damn CJD Questionnaire that they worked
> so hard, NOT to have. I firmly believe that CJD via the medical and surgical
> arena will play a huge roll in this down the road, if something is not done
> fast. I have corresponed with Julie Rawlings, Texas Department of Health
> Infectious Disease Epidemiology and Surveillance (IDEAS)
> jrawlings@discon.tdh.state.tx.us
> phone: (512) 458-7228 (512) 458-7676 FAX: (512) 458-7616
>
>
> thank you,
> with kindest regards,
>
> I am sincerely,
>
> Terry S. Singeltary Sr.
>
>
>
>
> USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN
>
> 18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
> December 2006 are now available.
>
>
> snip...
>
>
>
> 64. A member noted that at the recent Neuroprion meeting, a study was
> presented showing that in transgenic mice BSE passaged in sheep may be more
> virulent and infectious to a wider range of species than bovine derived BSE.
>
> Other work presented suggested that BSE and bovine amyloidotic spongiform
> encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
> prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
> MUTATION FOUND IN CASES OF SPORADIC CJD.
>
>
> snip...
>
>
>
> http://www.seac.gov.uk/minutes/95.pdf
>
>
>
>
> 3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse
>
> Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western
> Reserve
> University
>
> Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
> discovered recently in Italy, and similar or different atypical BSE cases
> were also reported in other countries. The infectivity and phenotypes of
> these atypical BSE strains in humans are unknown. In collaboration with
> Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
> inoculated transgenic mice expressing human prion protein with brain
> homogenates from BASE or BSE infected cattle. Our data shows that about half
> of the BASE-inoculated mice became infected with an average incubation time
> of about 19 months; in contrast, none of the BSE-inoculated mice appear to
> be infected after more than 2 years.
>
> ***These results indicate that BASE is transmissible to humans and suggest
> that BASE is more virulent than
> classical BSE in humans.***
>
>
> 6:30 Close of Day One
>
>
> http://www.healthtech.com/2007/tse/day1.asp
>
>
>
>
> SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
> 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
> of 'UNKNOWN' strain growing. ...
>
>
> http://www.cjdsurveillance.com/resources-casereport.html
>
>
>
> 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
>
>
>
> Diagnosis and Reporting of Creutzfeldt-Jakob Disease
>
> Singeltary, Sr et al. JAMA.2001; 285: 733-734.
>
> http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535
>
>
> BRITISH MEDICAL JOURNAL
>
> BMJ
>
> http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2
>
>
> BMJ
>
> http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1
>
>
> 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
>
>
> Conversion of the BASE Prion Strain
> into the BSE Strain: The Origin of BSE?
>
> Raffaella Capobianco1, Cristina Casalone2, Silvia Suardi1, Michela
> Mangieri1, Claudia Miccolo1, Lucia Limido1,
> Marcella Catania1, Giacomina Rossi1, Giuseppe Di Fede1, Giorgio Giaccone1,
> Maria Grazia Bruzzone1, Ludovico Minati1,
> Cristiano Corona2, Pierluigi Acutis2, Daniela Gelmetti3, Guerino Lombardi3,
> Martin H. Groschup4, Anne Buschmann4,
> Gianluigi Zanusso5, Salvatore Monaco5, Maria Caramelli2, Fabrizio
> Tagliavini1*
> 1 Fondazione I.R.C.C.S. Istituto Neurologico Carlo Besta, Milan, Italy, 2
> Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d’Aosta,
> Torino, Italy, 3 Istituto
> Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Brescia,
> Italy, 4 Friedrich-Loeffler-Institut, Institute for Novel and Emerging
> Infectious Diseases, Greifswald,
> Insel Riems, Germany, 5 Department of Neurological and Visual Science,
> Section of Clinical Neurology, Policlinico G. B. Rossi, Verona, Italy
>
> Atypical neuropathological and molecular phenotypes of bovine spongiform
> encephalopathy (BSE) have recently been
> identified in different countries. One of these phenotypes, named bovine
> ‘‘amyloidotic’’ spongiform encephalopathy
> (BASE), differs from classical BSE for the occurrence of a distinct type of
> the disease-associated prion protein (PrP),
> termed PrPSc, and the presence of PrP amyloid plaques. Here, we show that
> the agents responsible for BSE and BASE
> possess different biological properties upon transmission to transgenic mice
> expressing bovine PrP and inbred lines of
> nontransgenic mice. Strikingly, serial passages of the BASE strain to
> nontransgenic mice induced a neuropathological
> and molecular disease phenotype indistinguishable from that of BSE-infected
> mice. The existence of more than one
> agent associated with prion disease in cattle and the ability of the BASE
> strain to convert into the BSE strain may have
> important implications with respect to the origin of BSE and spongiform
> encephalopathies in other species, including
> humans.
>
> Citation: Capobianco R, Casalone C, Suardi S, Mangieri M, Miccolo C, et al.
> (2007) Conversion of the BASE prion strain into the BSE strain: The origin
> of BSE? PLoS Pathog 3(3):
> e31. doi:10.1371/journal.ppat.0030031
>
>
> Introduction
>
>
> snip...
>
>
> Although BASE showed a significant barrier to primary
> transmission to inbred mouse lines resulting in preclinical
> infection, it remains of considerable concern whether the
> causal agent is potentially pathogenic for humans. In this
> regard, the neuropathological and molecular features of
> BASE—in particular, the biochemical type and deposition
> patterns of PrPSc—have striking similarities with those of a
> distinct subgroup of patients with sporadic CJD [16]. This
> finding requires a cautious interpretation. Nonetheless, the
> possibility that the origin of CJD in some patients with a
> sporadic disease phenotype may be related to BASE exposure
> has to be considered and verified through transmission studies.
>
>
> see full text ;
>
>
> http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&blobtype=pdf&artid=1817656
>
>
>
> USA CJD QUESTIONNAIRE
>
> http://brain.hastypastry.net/forums/showthread.php?referrerid=38487&t=2408
>


snip...end...TSS




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